The to walk.2 Hypokinesia is characterized by decreases

The effects of Parkinson’s disease (PD) range from cognitive
to gait related impairments. The pathological issues result from the
destruction of dopamine producing neurons, affecting the basal ganglia. The Basal
ganglia is a group of neurons in the brain that work together and are responsible
for the quality of our movement and the execution of well learned tasks. The
lack of dopamine production adversely affects the basal ganglia, which in turn impairs
motor control in people with PD, leading to gait abnormalities.1

Cardinal symptoms of PD are marked by bradykinesia,
hypokinesia and gait akinesia.1 Bradykinesia is defined as slowness
of movement, which effects facial expressions, eye movements, and gait speed in
patients with PD.1 Gait akinesia results in freezing of gait (FOG),
a gait abnormality specific to this patient population, that commonly occurs in
doorways or while making turns. Individuals with FOG will ‘freeze’ while
walking or hesitate to walk.2 Hypokinesia is characterized by
decreases in the range and size of overall movement, affecting temporal,
spatial and kinematic components of gait.1 Tempo-spatial parameters
of gait include gait speed, step length, and stride length for example.
Kinematic parameters of gait include joint angular displacements. As PD progresses
these deficits worsen and the potential for fall risk increases, representing a
major challenge determining effective treatment interventions.2

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Rhythmic auditory stimulation (RAS) refers to a technique of
neurologic music therapy that uses rhythmic cues during gait training to
improve motor control.3 Patients affected by PD perform poorly in cognitive related tasks that
involve timing and execution of movements, like walking. Interventions based on
RAS provide patients with guidance pertaining to temporal processing, which
facilitates normal movements during gait.4 RAS treatment, along with gait
training can potentially prove to be an effective intervention for the PD population.3
The
processing that occurs in primary structures of the brain like the basal
ganglia, cerebellum and brain stem can be controlled by RAS treatment, thereby
bypassing the impaired structures of the brain.7

 

A
2016 quasi-experimental study by Pau et al, explored the effects of physical
rehabilitation integrated with RAS on spatio-temporal and kinematic parameters
of gait in people with PD. The study included 31 subjects initially, but only
26 subjects completed the study due to musculoskeletal injuries and
chemotherapy. The subjects of the study had mild to moderate PD disability
assessed via the Hoehn and Yahr scale. The intervention lasted 5 weeks and
included supervised treatment twice a week for 45 minutes, consisting of RAS
and exercises aimed to improve balance, mobility, and posture. The RAS
consisted of auditory beats that were personalized for each subject based on
their assessment before the start of the study. The results of the study showed
statistically significant improvement with the use of RAS on spatio-temporal
parameters including gait speed and step length and on kinematic parameters including
hip flexion and extension and ankle dorsi-plantarflexion. The authors
considered that the increase in overall gait speed was a large meaningful
effect, noted by an increase of 0.14 meters per second.4 Limitations
of the study included a lack of a control group, personalized RAS treatment,
and a low number of patients which prevent the results from being generalized.4
The authors admit that further studies, specifically randomized control
trials on RAS treatment and kinematic gait parameters needs to be conducted,
since spatio-temporal benefits have already been researched.4

A
2010 non-randomized control trial by Arias et al, looked at the effect of RAS
on gait in PD patients with and without freezing of gait episodes. As mentioned
earlier, this gait abnormality is specific to this patient population and
includes freezing in place while walking, commonly occuring in doorways or when
making turns.2 According to the authors of the study RAS is known
the help PD patients improve gait without freezing gait episodes, but effects
of RAS on PD patients with freezing gait has not been thoroughly evaluated. The
intervention was conducted for two consecutive days. Subjects were instructed to walk through a
corridor with a doorway, make pivot turns and touch buttons on the wall of the
corridor. These tasks were used in the study because they evoke freezing gait
episodes.5A portable device provided the auditory stimulation via
head phones. The study
included 10 PD subjects with freezing of gait episodes (PD+FOG), 9 PD subjects
without freezing gait episodes (PD-FOG) and 10 healthy subjects (used as a
control group).

The
first day consisted of 2 trials with and without RAS and the second day
consisted of 4 trials for the PD+FOG and PD-FOG group and 6 trials for the
control group with and without RAS. The authors remarked that trials were
conducted in this way to avoid
stimulation carryover effect.5 The number of freezing episodes, velocity, cadence, step length
and turn around time were analyzed. The main outcome of the study showed that freezing of gait episodes in
the PD+FOG group reduced significantly from 59 freezing episodes without RAS to
14 freezing episodes with RAS. Velocity, step length and turn around time were
also improved. Limitations included the short length of the study, number of
subjects, and lack of randomization.

 

A
2016 non-randomized control trial by Sangita, et al looked at the effect of RAS
in gait training among stroke patients. 30 subjects were divided into 2 groups
(15 subjects in each group). The control group received conventional
physiotherapy alone and the experimental group received RAS in addition to physiotherapy.
The intervention lasted 3 weeks. 
Subjects were evaluated for gait velocity through a ten meter walk test
and cadence (steps per minute).  Subjects
were assessed on the first day and last day of the treatment. Researchers found
that RAS treatment with physiotherapy lead to significant functional gains,
primarily an increase in gait speed in the experimental group versus the
control group.  The authors concluded
that rhythmic activity that involves highly repetitive and patterned movement inspires
the growth of neurons in the brain, improving physiological functions like
motor control, execution and cognitive function.6 The authors
present a case for the biological plausibility of RAS and it’s stimulation of
long term potentiation in sensory and motor cortex as a tool for motor learning,
with regards to stroke patients.6 Individuals with Parkinson’s
experience a general decline as the disease progresses over time, whereas
stroke patients generally improve and more than likely return to prior level of
functioning post stroke (depending on severity). Unfortunately, these results
cannot be generalized to include the PD population, but they explore the potential
benefits of RAS treatment on a biological level.  Limitations to this study included its short
duration, lack of randomization, and its target population did not include PD
subjects.

Previous
research has explored and demonstrated the efficacy of RAS for the improvement
of gait abnormalities in individuals with PD and other neurological diseases.3,6
However, after a review of the literature, RAS is only effective on temporal
and spatial parameters of gait. The effects of RAS on the kinematic parameters
of gait is sparse and more research needs to be conducted. Individuals in the
reviewed studies had PD in varying stages and with specific gait abnormalities.
Research specific to PD stage of disease, gait related deficits and RAS
treatment should also be explored. The literature did reveal that RAS treatment
efficacy can span multiple neurological diseases that affect motor control and
mechanisms of gait. The purpose of this literature review was to examine the
efficacy of RAS on gait abnormalities in people with Parkinson’s disease. 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

References

1.      
Mazzoni P, Shabbott B, Cortés JC.
Motor Control Abnormalities in Parkinson’s Disease. Cold Spring Harbor Perspectives in Medicine.
2012;2(6):a009282. doi:10.1101/cshperspect.a009282.

 

2.      
Grabli D, Karachi C, Welter M-L, et
al. Normal and pathological gait: what we learn from Parkinson’s disease. Journal of neurology, neurosurgery, and psychiatry.
2012;83(10):10.1136/jnnp-2012-302263. doi:10.1136/jnnp-2012-302263.
 

3.      
 Kim S, Kwak E, Cho S, et al. Changes in gait
patterns with rhythmic auditory stimulation in adults with cerebral
palsy. Neurorehabilitationserial online. September
2011;29(3):233-241. Available from: CINAHL Plus with Full Text, Ipswich, MA.
Accessed December 7, 2017.

4.      
Pau M, Corona F, Pili R, et al. Effects of Physical
Rehabilitation Integrated with Rhythmic Auditory Stimulation on Spatio-Temporal
and Kinematic Parameters of Gait in Parkinson’s Disease. Frontiers in
Neurology. 2016;7:126. doi:10.3389/fneur.2016.00126.

5.      
Arias P, Cudeiro J. Effect of Rhythmic Auditory Stimulation
on Gait in Parkinsonian Patients with and without Freezing of Gait. Gwinn K,
ed. PLoS ONE. 2010;5(3):e9675. doi:10.1371/journal.pone.0009675.

6.      Sangita K, Remya N. The Effect of Rhythmic Auditory Stimulation in
Gait Training among Stroke Patients. Indian Journal Of Physiotherapy
& Occupational Therapy serial online. October 2016;10(4):61-66.
Available from: CINAHL Plus with Full Text, Ipswich, MA. Accessed December 7,
2017.

7.      
M.H.
Thaut, Neural basis of rhythmic timing networks in the human brain, Ann N Y
Acad Sci 999 (2003), 364–373