Insights on Management of Parkinson Gait

Oct 07, 2006

Parkinson gait is characterized by shuffling, including a decreased stride length and gait speed. The diminished stride and gait speed coupled with increased cadence puts the patient at risk for postural instability resulting in falls.

Parkinson gait is characterized by shuffling, including a decreased stride length and gait speed. The diminished stride and gait speed coupled with increased cadence puts the patient at risk for postural instability resulting in falls. Hip flexion contracture, hamstring muscle length, 6- and 10-meter walk distance, and turning while standing are physical performance tasks that require evaluation in the patient with Parkinson disease (PD) and become the therapeutic focus for gait stabilization.1 Auditory stimulus training and visual cues are some of the techniques used in gait stabilization. Furthermore, gait training can be optimized by coordinating practice with medication on/off cycles.

RESEARCH ON GAIT INSTABILITY IN PD

  • Passingham2 reported that step initiation correlated with sensory information feedback from the basal ganglia. Because of the resultant motor disturbance in the basal ganglia-sensorimotor feedback loop, the patient with PD requires external cues to achieve appropriate velocity, cadence, and step length in gait.
  • A study by Morris and colleagues3 demonstrated that for step initiation to occur without postural instability, gait velocity, step length, and cadence must be a coordinated event. They performed 3 test conditions in 34 patients with PD and 34 matched controls. The results of the study demonstrated that stride length did not correlate with a fixed cadence when internal cueing was used; however when stride length was fixed and cadence allowed to modulate with internal cues, a correlation was seen. This study supported the concept that gait hypokinesia in PD results from deficits in stride length regulation.
  • Martin and colleagues4 reported on gait initiation and postural instability in patients who had Hoehn and Yahr PD rating scale scores of 1 to 3. The researchers found that vertical forces control the center of mass (COM) distance, while posterior and lateral forces regulate the center of pressure (COP) distance.
  • Jian and colleagues5 demonstrated that patients with PD compensate for a lack of postural stability by decreasing the COM-COP ratio to create stability in gait. They reported that COP moves backward, forward, and medial as forces are displaced onto the lower extremity from swing to stance phase to toe-off in gait. They also noted that the COM-COP ratio is important in chair rise, stair climbing, and gait initiation. Compared with younger and older healthy controls, COM in patients with PD was reduced by 50% and 20%, respectively.

IMPACT OF MEDS ON GAIT
Gait is improved during the on phase of levodopa therapy.6,7 A study by Morris and colleagues6 on temporal stability of gait showed that gait became stabilized for about 2½ hours following administration of levodopa. A study by Burleigh-Jacobs and colleagues7 showed that peak swing limb, COM velocity, anticipation, and push-off phases during the on phase of the medication cycle were 71%, 93%, 100%, and 116% that of controls, respectively.

In my experience, intervention is more successful if medication is taken in the morning shortly before presenting for physical therapy. Attention span and ability to concentrate on motor tasks is better, and patients experience less bradykinesia and freezing.

REHABILITATIVE GAIT TRAINING
In working with a small number (7) of ambulatory patients with PD (age range, 70 to 80 years), we achieved a 5% to 7% positive change in gait and step length. The rehabilitation protocol involved repetitive training in a 10-meter walk. The walks were practiced without assistive devices across 12 inches of a linoleum floor. Contact guard assistance, as needed, and a gait belt were provided to ensure patient safety. Colored strips were placed perpendicularly along the walkway to note clinical change from pre- and post-testing for step length. The treatment intervention also involved a home exercise program of stretching, strengthening, gait, and balance exercises that helped keep the patient active, prevented stiffness, and increased strength.

Visual and Auditory Cues
Visual cues consist of lines, markers, or strips oriented in a specific direction on the floor. Their purpose is to improve patient awareness of gait speed and step length. Patients are taught to look at the spaced cues on the floor and replicate the step length in the gait cycle.

Morris and colleagues8 reported that cognition and fixation are key factors in motor learning behavior. Fixation gives way to an automatic response once the skill is learned. The researchers hypothesized that incomplete retention of walking skill caused by motor disruption in the basal ganglia may be the reason patients with PD remain in a fixation phase of learning gait.

In another study, Morris and colleagues9 showed that external cues are necessary in treating gait dysfunction. The researchers found that both preferred walking (ie, comfortable gait speed) and fast walking in patients with PD was 75% of that of normal age-matched controls. The gait parameters of velocity, cadence, and step length for fast walking were greater than 95% that of normal values when visual cues were used.

Rhythmic auditory stimulus (RAS) training also can improve functional locomotor patterns in walking.10,11 Rhythmic auditory stimulation training involves timed cues such as a click, beat, or tap given at specific intervals for learning a sequential activity. It helps integrate the components of gait function.

Electromyography has been useful in monitoring progress in RAS training.10-12 Miller and colleagues12 evaluated PD gait using electromyography to determine muscle symmetry and variability of the lower leg muscles in patients receiving RAS training. A 34% and 4% reduction, respectively, in electromyographic (EMG) asymmetry of the medial gastrocnemius and tibialis anterior muscles was demonstrated in 8 patients who had Hoehn and Yahr PD rating scale scores of 2 to 3 after 3 weeks of RAS training. In addition, a 58% and 60% reduction, respectively, in EMG shape variability for the tibialis anterior and medial gastrocnemius was seen. The reductions in EMG shape variability correlated with a 30% and 13% increase in walking speed and stride length.

A study by Thaut and colleagues10 also demonstrated significant changes in EMG symmetry when RAS was used for home-based training (P < .005). In addition, McIntosh and colleagues11 found that RAS training resulted in significant improvement over baseline in mean values for gait velocity, cadence, and step length (P <.05).

CONCLUSION
Gait hypokinesia in PD results from a fundamental deficit in the ability to regulate step length. Shorter step length leads to balance instability and subsequent risk of falls and injuries. Positive clinical outcomes in gait training can be achieved through use of verbal and auditory cues and awareness of patients' on-off medication cycles. In my view, an eclectic approach that emphasizes safety, home exercises for gait and balance, and repetition is the most successful.

LOUIS GRANT, PT, ATC, is an outpatient physical therapist withSouthwest Regional Rehabilitation Center in Battle Creek, Michigan.

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3. Morris ME, Iansek R, Matyas TA, et al. The pathogenesis of gait hypokinesia in Parkinson's disease. Brain. 1994;117:1169-1181.
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9. Morris ME, Iansek R, Matyas TA, Summers JJ. Ability to modulate walking cadence remains intact. J Neurol Neurosurg Psychiatry. 1994;57:1532-1534.
10. Thaut MH, McIntosh GC, Rice RR, et al. Rhythmic auditory stimulation in gait training for Parkinson's disease patients. Mov Dis. 1996;11:193-200.
11. McIntosh GC, Brown SH, Rice RR, et al. Rhythmic auditory-motor facilitation of gait patterns in patients with Parkinson's disease. J Neuro Neurosurg Psych. 1997;62:22-26.
12. Miller RA, Thaut MH, McIntosh GC, Rice RR. Components of EMG symmetry and variability in parkinsonian and healthy elderly gait. J Electroenceph Clin Neurophys. 1996;101:1-7.

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