Gait disorders and balance disturbances in Parkinson’s disease:
clinical update and pathophysiology
Tjitske A. Boonstraa,b, Herman van der Kooijb,c, Marten Munnekea
and Bastiaan R. Bloema
Parkinson’s disease is an incapacitating disease that
negatively affects the quality of life for many reasons,
not the least of which is the presence of axial disability
(gait disorders, balance impairment, falls and fall-related
injuries) [1??,2]. Here, we review recent clinical and
fundamental studies dealing with gait, balance and falls
of January 2006 until February 2008. First, we provide an
overview of the epidemiology and clinical significance,
followed by recommendations on clinical assessment
techniques. We subsequently discuss new pathophysio-
logical insights, aiming specifically at turning strategies,
the relevance of asymmetries in axial motor control and
impaired sensorimotor integration. We also highlight
developments in the field of neuroimaging. Treatment
issues are covered next, focusing on drug treatment, deep
brain stimulation[in particularpedunculopontine
nucleus (PPN) stimulation] and physiotherapy. We con-
clude by providing recommendations for future research.
Recent studies have confirmed the high rate of falls in
Parkinson’s disease. Additionally, risk factors and pre-
dictors for falls were identified.
Prevalence and clinical impact
Prior studies on falls in Parkinson’s disease included
relatively small patient groups. A recent meta-analysis
addressed this by pooling the results of six independent
prospective studies of falling in Parkinson’s disease [1??].
The pooled sample size included 473 patients. The
3-month fall rate was 46% (95% confidence interval:
38–54%). Interestingly, even among patients without
prior falls, this fall rate was substantial (21%, 12–35%).
aDepartment of Neurology, Donders Center for
Neuroscience, Radboud University Nijmegen Medical
Centre, Nijmegen,bDepartment of Biomechanical
Engineering, University of Twente, Enschede and
cDepartment of Biomechanical Engineering, Delft
University of Technology, Delft, The Netherlands
Correspondence to Dr Bastiaan R. Bloem, Associate
Professor of Neurology, Medical Director, Parkinson
Center Nijmegen (ParC), Department of Neurology,
935, Radboud University Nijmegen Medical Centre,
PO Box 9101, 6500 HB Nijmegen, The Netherlands
Tel: + 31 24 3615202; fax: + 31 24 3541122;
Current Opinion in Neurology 2008, 21:461–471
Purpose of review
Parkinson’s disease. Here, we discuss the latest findings regarding epidemiology,
assessment, pathophysiology and treatment of gait and balance impairments in
Recent studies have confirmed the high rate and high risk of falls of patients with
Parkinson’s disease. Therefore, it is crucial to detect patients who are at risk of falling
the prediction of falls in Parkinson’s disease. Difficulty turning may be caused by axial
rigidity, affected interlimb coordination and asymmetries. Turning difficulties are easily
assessed by timed performance and the number of steps during a turn. Impaired
sensorimotor integration, inability of switching between sensory modalities and lack of
compensatory stepping may all contribute to the high incidence of falls in patients with
Parkinson’s disease. Similarly, various studies highlighted that pharmacotherapy,
neurosurgery and physiotherapy may adversely affect balance and gait in Parkinson’s
Insights into the pathophysiology of Parkinson’s disease continue to grow.
At the same time, it is becoming clear that some patients may in fact deteriorate with
treatment. Future research should focus on the development and evaluation of
multifactorial fall prevention strategies.
balance, deep brain stimulation, falls, freezing, Parkinson
Curr Opin Neurol 21:461–471
? 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
1350-7540 ? 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
These results underscore that patients with Parkinson’s
disease have a high risk of falling, even when they have
in the Sydney multicenter study , in which 136 newly
diagnosed patients with Parkinson’s disease were fol-
lowed for 20 years . Of the 36 survivors, 87% had experi-
enced falls and 35% had sustained (multiple) fractures
(Fig. 1). These falls occurred despite maximal treatment
with levodopa, confirming earlier impressions that axial
disability in late stage Parkinson’s disease is largely dopa-
resistant (likely due to extranigral and nondopaminergic
brain lesions). The high risk of fractures was also demon-
strated in a large case–control study , which showed
that patients with parkinsonism (not just Parkinson’s
disease) had a more than two-fold increased risk of
sustaining any fall-related fracture. Interestingly, levo-
dopa was paradoxically associated with an increased over-
all risk of fractures, especially hip fractures. One possible
explanation is that levodopa dose was merely a marker of
disease severity, or that levodopa caused adverse effects
that predisposed patients to falls, for example, violent
dyskinesias or drug-induced orthostatic hypotension .
Another option is that patients on levodopa are simply
more mobile and, therefore, more prone to fall. Indeed,
fall rates tend to taper with disease progression, likely
because patients become increasingly immobilized [1??]
and thereby ‘protect’ themselves from further falls.
The negative impact of gait disorders on quality of life is
falling. ‘Episodic’ gait disorders – which are only inter-
mittently present – are particularly incapacitating
because patients cannot easily adjust their behavior to
these paroxysmal walking problems [4?]. A textbook
example is freezing of gait (FOG), in which patients
with Parkinson’s disease experience debilitating epi-
sodes during which they are unable to start walking
or – while walking – suddenly fail to continue moving
forward. Because of this sudden and unpredictable
nature, FOG is an important cause of falls and injuries.
Perhaps not surprisingly, a recent study  showed that
FOG was independently associated with a decreased
quality of life.
Risk factors and predictors
To predict patients (and in particular prior nonfallers)
who are most likely to fall next remains difficult; these
persons, however, would be ideal candidates for an
intensive fall prevention program. In the aforementioned
meta-analysis [1??], the best predictor of falling was two
or more falls in the previous year (which is unsatisfactory
as predictor because patients have already begun falling),
and even this had a relatively modest predictive ability
(sensitivity only 68%; specificity acceptable at 81%).
Interestingly, among prior nonfallers, fear of falling had
a moderate sensitivity in predicting falls, so maybe
people sense their own instability before doctors can
detect this physically. Fear of falling can be evaluated
using the Activities-specific Balance Confidence (ABC)
scale, which has been validated for use in Parkinson’s
disease and, more recently, also in abbreviated form
(using only six of the original 16 questions) [6,7]. Fear
of falling was also associated with prior falls in another
study , although the strongest determinants of falls
were impaired ambulation, impaired lower-limb motor
planning and, interestingly, orthostasis. The relevance of
review , exploring the relation between clinical fea-
tures and falls and fractures in pathologically diagnosed
patients. Among confirmed patients with Parkinson’s
disease, autonomic instability was one of the few factors
that independently predicted the time to the first fall.
Falls due to syncope are thought to be uncommon in
Parkinson’s disease , but these two studies suggest
that clinicians may perhaps miss relevant orthostatic
Figure 1 Kaplan–Meier plot of time to falls, dysphagia, symptomatic postural hypotension, and first fracture
Time to event
Adapted from . First fall;Hypotension; Dysphagia; First fracture.
hypotension in some patients, either because it is simply
not measured or because clinical ascertainment is not
infallible . Another potentially interesting predictor
overt falls [1??], but more work is needed to develop clear
definitions and a reliable way of ascertaining near-falls.
Clinical and quantitative assessment of axial disability
Several researchers have developed methods to assess
gait, FOG, postural instability and balance confidence
focused on predicting falls in Parkinson’s disease [12–14].
New insights were gained in the area of turning, axial
asymmetry, sensorimotor integration impairments and
Patients with Parkinson’s disease often have difficulty
turning around, not only while lying recumbent in bed,
but also while standing upright. These turning problems
have great clinical relevance because of the relation with
FOG and hip fractures. It would be helpful to have
simple tools to detect turning difficulties, to estimate
the risk of falling and to record the outcome of thera-
peutic interventions. Several recent studies [23–26]
have shown that simply a timed performance and count-
ing the number of steps during a 180 degree axial turn
may suffice, as patients with Parkinson’s disease require
more steps and also turn slower than controls.
Quantitative measures may assist clinicians in evaluating
these turning difficulties, and this would be particularly
Gait and balance in Parkinson’s disease Boonstra et al.
Table 1 Overview of new assessment techniques to measure axial disability (gait, balance, posture and falls) in Parkinson’s disease
Technique Type Main outcomeRemarks/critique Reference
ABC-6 (shortened version
of ABC-16, a questionnaire
focused on fear of falling)
Clinical A shortened version of the
ABC-16, featuring only six
of the original 16 questions, is a
valid tool to assess fear of falling
Improved prediction of falls in
PD, compared to individual tests
Less interrater variability and better
prediction of self-reported prior falls
Minor variants may exist
between different countries
Combination of multiple
clinically based balance testsa
‘Push and release’ test (variant to
the commonly used pull test)
Clinical Ideal combination remains
Relation to prospectively
documented falls unknown;
some patients experience
the test as threatening
Generic scale which fails to
features, such as asymmetrically
reduced arm swing or turning
‘en bloc’; relation to historical
falls only moderate, and relation
to prospectively documented
Utility at individual patient level
not determined; feasibility for
use in clinical practice remains
Requires independent confirmation
Tinetti mobility testClinical Interrater and intrarater reliability
good to excellent; moderate
relation to faller status
Quantitative kinematic gait analysis Quantitative At the group level, significant
differences between patients and
controls, and within patients before
versus after rehabilitation
Quantitative Good consistency and interrater
reproducibility, closely related to
clinical scales and ablity to change
Quantitative PCI measures interlimb coordination
Quantitative Reliable detection of stride length and
motor fluctuation due to levodopa
therapy in the home situation
Quantitative 89% sensitivity for the detection of
freezing, with 10% false negatives,
after individual calibration in a
Global mobility task: qualitative
and quantitative assessment
of ability to roll over on the
floor and stand up in five steps
Phase coordination index (PCI)
Feasibility for use in clinical practice
remains to be determined
Other symptoms of PD, such as
tremor and bradykinesia cannot be
detected with the stride monitor
Individual calibration is needed.
Discussion remains about the
frequency of freezing. Feasibility
for the home environment needs
to be determined
Requires a GAITRite system to
quantitatively assess gait
Ambulatory gait assessment, using
goniometers on the shank
Ambulatory freezing assessment
using goniometers on the shank
GAITRite system Quantitative The GAITRite system is an effective and
efficient method to evaluate parkinsonian
bradykinesia. Also, it is possible to use
the system as a substitute for the
traditional timed tests
aDibble et al., (2006) and Dibble et al., (2008): Functional reach test, Berg balance scale, dynamic gait index, timed up and go and the cognitive timed
upand go tests. Jacobset al., (2006): One-legstance test, functionalreach test, and the UPDRSmotorexam. Fearof fallingwas assessed by the ABC
scale and participants reported how many times they fell during the previous year.
in Parkinson’s disease [19?,21?,27]. For example, it was
shown that turn duration is longer in patients with Par-
peak roll angular velocity of the trunk were reduced in
used for clinical examination in single patients, or as
objective outcome measure of axial turning or FOG in a
domestic setting, for example, in intervention studies.
Turning problems may result from inability to adequately
difficultduringturningwhen – bynecessity – thetwolegs
ant factor is axial ‘stiffness’ and loss of intersegmental
flexibility. One study [31?] measured trunk resistance to
in Parkinson’s disease. Importantly, levodopa gave no
improvement, again suggesting that axial disability is lar-
gely dopa-resistant, unlike the ‘appendicular’ movements
(hand control), which appear to be controlled by separate
dopaminergic neural systems. Two other studies [24,30]
showed a loss of intersegmental axial coordination in Par-
kinson’s disease, which corresponds to the well known
clinical phenomenon of ‘en bloc’ turning in this disease.
A new factor that may contribute to postural instability
was identified in 11 patients with Parkinson’s disease
with unexplained unsteadiness. Polygraphic recordings,
including surface electromyography (EMG), showed an
orthostatic tremor of varying frequency (ranging from 4 to
18Hz) in eight patients and, interestingly, a hitherto
undiscovered orthostatic myoclonus in the remaining
three patients . The findings also had treatment
implications: patients with fast tremor improved on
clonazepam, whereas patients with slow tremor or myo-
clonus improved on levodopa, and sometimes benefited
further when clonazepam was added.
Asymmetries in gait and posture
By definition, Parkinson’s disease is an asymmetrical dis-
ease. A unique study on 35 ‘de-novo’ patients with
Parkinson’s disease who were not yet treated with any
antiparkinsonian medication  showed that asymme-
tries in gait (detected with simple pressure-sensitive
insoles) are also an inherent symptom of early stage
Parkinson’s disease, and not merely a side effect of medi-
cation or a late disease complication. Interestingly, this
asymmetry was presenteventhoughstride-to-stride varia-
bility (previously thought to be one of the most sensitive
measures of gait changes in Parkinson’s disease) was
normal in these early patients. Moreover, subtle asymme-
tries in balance control can be detected in Parkinson’s
disease by carefully analyzing the independent contri-
bution of both legs to stance control, even before these
changes are detected with the naked clinical eye .
Cognitive influences on gait and balance
An important new insight is the recognition that walking
and standing are not purely automatic tasks, regulated by
subcortical control mechanisms and requiring little if any
conscious attention. Instead, gait is now increasingly seen
as a complex ‘higher-order’ form of motor behavior, with
prominent and varied influences of mental processes
[34??]. For example, this becomes evident under complex
circumstances, whenpatientswith Parkinson’s diseaseare
unable to deal with multiple tasks simultaneously, either
because the central processing abilities have become too
limited, or because patients fail to properly prioritize their
balance control over other, less important secondary tasks,
placing patients at a higher risk of falling .
Most investigators would regard postural instability as
being caused by disturbed motor programing of postural
corrections within the basal ganglia (‘efferent’ deficit).
However, this view has been challenged by observations
partially due to central proprioceptive disturbances
(‘afferent’ deficit). Thus far, proprioceptive disturbances
have mostly been demonstrated for arm movements,
including for example, defective kinesthesia, defective
joint position sense or disturbed tactile spatial acuity.
Recent work suggests that afferent (mainly propriocep-
tive) disturbances could also play a role in the pathophy-
siology of postural deficits in Parkinson’s disease. For
example, one study [36?] perturbed standing patients
with Parkinson’s disease using very slow horizontal sinu-
soidal oscillations of a supporting platform, delivered at
an amplitude and frequency that was kept below the
semicircular canal perception threshold (i.e. patients
were dependent on proprioceptive feedback to maintain
balance). Patients swayed abnormally under these cir-
cumstances, but were able to partially correct this using
visual feedback. Interestingly, this switch from kines-
thetic-dependent to vision-dependent balance control is
slower in patients with Parkinson’s disease compared
with controls, suggestinga difficulty in changing between
different sensory modalities – an ability that is much
needed in everyday life with its constantly changing
environment [37,38?]. Another group showed that the
responsetotendonvibration – awaytodeceivethemuscle
spindles and create a false sensation of muscle stretch – is
and does not habituate well, resulting in changed patterns
of body sway [39,40]. Such somatosensory deficits may
produce an abnormally constructed body scheme and
explain, for example, the stooped posture of patients
with Parkinson’s disease, of which they are often subjec-
tively unaware . This concept was confirmed by an
interesting study [42?] in which patients with Parkinson’s
disease were asked to perform a Functional Reach task
(extending the arm forward as far as possible, with both
feet fixed at the floor). Patients with Parkinson’s disease
tended to overestimate their limits of stability, and this
may be related to their falling tendency in everyday
balance correcting strategies to prevent patients from fall-
Various studies [43,44?] addressed the nature of compen-
satory stepping and showed that patients with Parkinson’s
disease have difficulties initiating a compensatory step. A
newly emerging concept is that failure to initiate compen-
postural adjustments (a lateral weight shift is normally
required to allow for a contralateral limb swing) [44?].
The fascinating inference is that a walking problem (gait
is, the inability to shift weight. A related and equally
interesting finding showed that patients with Parkinson’s
disease, when provided with an assistive (externally
imposed) anticipatory postural adjustment, could step fas-
ter . One report showed that visual inputs may also
ameliorate compensatory stepping: patients with Parkin-
son’s disease took longer steps when a visual target was
provided, but performancedeteriorated whenparticipants
the importance of visual feedback to compensate for
motor disabilities in Parkinson’s disease (see section on
Structural and functional neuroimaging are used increas-
ingly to better understand the pathophysiology associ-
ated with gait and balance impairment in Parkinson’s
disease. An example of a structural imaging study – using
magnetic resonance imaging (MRI) – showed that, in
contrast to tremor, axial deficits were related to increases
in ventricular volume in Parkinson’s disease, but this
association was accounted for by age .
investigate the cerebral-based gait impairment in Parkin-
son’s disease. This approach has the considerable advan-
tage of perfectly matched ‘performance’ across different
patient groups (assuming that pathological alterations in
but also during rest). One study  used N-isopropyl-
p[123I] iodoamphetamine single photon emission com-
puted tomography (SPECT) to compare cerebral blood
flow between patients with either the ‘tremor-dominant’
subtype or the ‘postural instability and gait difficulty
(PIGD)’ subtype of Parkinson’s disease. The results
showed hypoperfusion in the anterior cingulate cortex
and primary visual cortex, but only in the PIGD group.
The frontal reduction in perfusion is particularly interest-
ing in light of the aforementioned relation with frontal
executive deficits [34??]. A further study used PET ,
2[18F]fluoro-D-glucose-PET (FDG-PET) – to measure
striatal glucose uptake – and 18[F]-6-fluoro-levodopa
(FDOPA)-PET – to measure striatal decarboxylase
activity – was measured in patients with Parkinson’s dis-
ease with and without FOG. In patients with FOG, lower
putaminal FDOPA uptake with increased FDG uptake
was observed, whereas caudate uptake of both FDG and
general problem in interpreting such studies is the match-
ing between subgroups. Ideally, the only difference
between groups would be their gait problems, and this is
difficult to achieve because gait is closely related to other
relevant variables such as disease severity and disease
duration. This is illustrated by the above-cited papers, in
which subgroups were not matched for disease severity or
disease duration [46,47].
Motor imagery of gait is a new approach to partially
circumvent the problems associated with functional ima-
ging of gait, assuming that imagined walking shares at
leastsome ofthe cerebral processeswithgait, but without
the need to engage in actual gait. Several groups have
developed paradigms for this [49,50]. In such studies, it is
crucial to verify performance and ascertain that patients
are actually specifically engaged in motor imagery of gait,
for example, by testing whether imagined movement
times increase as a function of distance that patients
are requested to travel. This approach has been used
successfully in healthy individuals [49,51] and is now
ready for application in Parkinson’s disease.
New insights were gained in the field of pharmacother-
apy, deep brain stimulation and physiotherapy. A brief
discussion of recruitment issues and guidelines for
randomized controlled trials (RCTs) is given.
Gait and balance problems in Parkinson’s disease tend to
be perceived as being ‘untreatable’, but there are various
therapeutic options . For example, one report showed
increases with time, these deficits do not become unre-
the seminal ELLDOPA study (a placebo-controlled trial
comparing various doses of levodopa) , which showed
that FOG was most common in the placebo group and
Gait and balance in Parkinson’s disease Boonstra et al.
low-dose levodopa group, compared with groups taking
higher levodopa dosages. However, levodopa may also
adversely affect gait or balance control. For example,
one study  showed that timing of gait to an external
stimulus was worse in medicated patients compared with
to drug-induced dyskinesias. Patients with Parkinson’s
disease using neuroleptics have an increased risk of sus-
to prove (patients requiring neuroleptics may simply have
more advanced disease). A new approach is methylpheni-
date (traditionally used to combat attention-deficit-
risks in community dwelling older adults, conceivably by
attention . Three further trials have now shown
that methylphenidate also improves gait and FOG in
Parkinson’s disease [57–59].
Bilateral subthalamic nucleus (STN) stimulation is an
effective treatment for Parkinson’s disease, especially
for appendicular symptoms that responded well to levo-
dopa preoperatively. However, the effects of STN stimu-
lation on axial motor signs remain debatable. It is imposs-
ible to draw overriding conclusions because of the
differences in surgical techniques, candidates selected
for surgery and outcome measures used. A few tendencies
are worth reporting. First, it has been suggested that
medication and deep brain surgery may affect axial mobi-
lity deficits by acting on different neural systems. Indeed,
some studies [60–62] reported improvement in postural
deficits, beyond the effects afforded by medication alone.
may act via ‘downward’ projections onto the PPN .
Second, there are increasing concerns that deep brain
stimulation may worsen axial mobility, sometimes as an
immediate adverse effect of surgery, but also as a long-
term complication. For example, one report showed that
after a 3-year follow-up of 36 patients with Parkinson’s
disease, STN stimulation had improved the United Par-
kinson’s Disease Rating Scale (UPDRS) motor score by
54.2% and gait scores by 45.3%, but dopa-unresponsive
axial signs had worsened in some patients . Another
study  investigated gait changes after STN stimu-
lation and found that gait had improved in half the
patients, but had worsened in the others. This inconsist-
ent response was also found in a dynamic posturography
study  that assessed postural control in patients with
Parkinson’s disease exposed to a random mix of multi-
directional tilts of a supporting forceplate. Participants
were tested with their STN stimulators switched on and
off, 60–90min after a suprathreshold dose of levodopa.
Overall balance – defined as displacement of the center
ofmassfollowingtheposturalperturbation – improved in
nine patients but deteriorated in the remaining four
patients. A particular worry is the development of new
gait and balance deficits several years after surgery, even
motor control. This was demonstrated in a study that
used a standardized questionnaire to ask patients about
both their global outcome and gait, at 6 months post-
operatively and at the time of examination (about
2.7 years postoperatively) (van Nuenen BF, Esselink
RA, Munneke M, et al. Secondary gait deterioration after
bilateral subthalamic nucleus stimulation in Parkinson’s
disease. Mov Disord 2008, in preparation). A striking 42%
of patients experienced a worsening of gait in the medi-
cation OFF phase, and this appeared to be fairly selective
because global outcome scales continued to be improved.
A major drawback of this study was the lack of control
group; hence some postoperative gait problems could
have been ascribed to natural disease progression.
An important target for future research is the develop-
ment of reliable determinants for success or failure of
deep brain surgery. It has been speculated that variability
in electrode placement can explain the inconsistent
effects on axial mobility across patients. Specifically, it
could be that misplaced electrodes project unintention-
ally to the PPN  which, when stimulated at high
frequencies, worsens gait and balance [66??,67]. This
hypothesis was addressed in an interesting study of 13
patients with Parkinson’s disease with severe postopera-
tive gait disorders [68??] whose typical stimulator settings
(130Hz) were changed to a much lower frequency of
60Hz, while keeping the total energy delivered constant.
All outcome measures (including UPDRS, a timed walk-
ing task and FOG) clearly improved during the 60Hz
nationputforwardwas that,because thePPNisjust5mm
away from the STN, high-frequency STN stimulation
could negatively affect the PPN (and the opposite for
low-frequency STN stimulation of course). On the basis
of these findings, the authors proposed a two-staged STN
frequency optimization: 130Hz during the initial years of
STNstimulation; and60Hz(at a higher voltage)after gait
disorders have become manifest.
Others examined the merits of direct PPN stimulation.
Smaller previous studies had shown the technical feasi-
bility of this approach, but interesting new insights came
from a study of six patients with Parkinson’s disease
[66??] whose gait and balance responded unsatisfactorily
to drug treatment, and therefore underwent bilateral
implantation of electrodes in both the STN and PPN.
The most interesting results were seen during the medi-
cation ON phase, when an extra treatment push (i.e. over
and above optimal drug therapy) is mostly needed.
During this ON state, PPN stimulation alone had a
positive effect on the UPDRS items for gait and balance,
whereas STN stimulation did not. PPN stimulation
improved axial symptoms directly postoperatively and
this persisted for 6 months. However, an extended fol-
low-up is needed to evaluate the long-term effects. An
important critique was that the electrodes might have
been misplaced, that is, not in the PPN, but rather in the
nucleus peripeduncularis . Therefore, the obtained
results should be interpreted with care, and further
research is needed to investigate the effects in more
detail (e.g. using objective measures such as posturogra-
phy), to study the effects of electrode (mis)placements
and to evaluate long-term effects.
Many patients with Parkinson’s disease receive phy-
siotherapy to alleviate symptoms of the disease. Here,
we review the most recent findings of studies investi-
gating treatments such as cueing and different forms
It is widely appreciated from clinical experience and
experimental, mainly lab-based studies that patients with
Parkinson’s disease can improve their gait using external
cues. In a seminal study for the field of physiotherapy,
this knowledge was taken to the test in a large, multi-
center and single-blind crossover study (RESCUE trial)
[70??] that examined the effect of a 3-week training
program, featuring three rhythmic cueing modalities:
visual, auditory or tactile. Immediately after the training
period, small but significant improvements were found
for clinical gait and balance scores, for FOG severity
(among freezers), for gait speed and step length, and
for timed balance tests [including the confidence to carry
out functional activities, as measured with the falls
efficacy scale (FES)].
Knowing whether beneficial effects persist after training
has ended is crucially important if one wants to imple-
ment cueing as treatment into clinical practice. In a lab-
based study , improvements in gait after rhythmic
auditory stimulation persisted at 2 and 15min after actual
the RESCUE trial [70??], the observed improvements
were no longer present in the noncued situation 6 weeks
after training. Note that assessments were carried out in
the absence of cues, whereas in daily life patients with
Parkinson’s disease will specifically use cues under those
circumstances in which they need them. Therefore, the
results found in the RESCUE trial might be an under-
estimation of the real effect when using cues.
Another relevant issue is a possible carry over of specific
training effects to other, nontrained tasks. Encouraging
completed a 4-week training program in which they prac-
showed significant improvements following this nonspe-
cific training. In contrast, the much larger RESCUE trial
such as functional outcome measures or quality of life.
A further issue – again with great clinical relevance – is
the emerging insight that cueing can also have adverse
effects. For example, one study  showed that rhyth-
mic auditory stimulation can differentially affect freezers
and nonfreezers. Specifically, the results showed that
rhythmic auditory stimulation (set at 110% of preferred
walking speed) afforded increases in step length for
nonfreezers, but produced the opposite effect for free-
zers. Another study  showed that visual cueing may
also adversely affect gait, depending on disease severity.
Falls may paradoxically increase when patients receive
cueing treatment, simply because mobility improves, and
also because the cueing may distract patients from paying
attention to environmental hazards. Fortunately, cueing
was not associated with more falls in the RESCUE trial
[70??], although the study was not properly powered to
address this issue. The take home message is that cueing
should not be prescribed as a ‘one size fits all’ treatment,
but should be carefully tailored to specific factors such as
disease severity and individual symptomatology.
A final practical concern is whether cueing – even when
conditions – will also benefit patients in daily life with its
complex situations, typically requiring patients to deal
with multiple tasks simultaneously. This was addressed
in two studies that showed that auditory cues helped to
improve walking speed during a dual task situation (e.g.
walking with filled cups on a tray), whereas somatosen-
sory cues (vibration on the wrist) had no effect, and visual
cues (a light emitting diode attached to the patient’s own
spectacles, or a pair of clear glasses) had a negative effect.
that rhythmic auditory cues had no effect in a single task
situation (normal walking) [75,76]. Perhaps participants
were challenged more during the dual task, with heigh-
information during the complex tasks . External cues
could theoretically reduce attentional loads by reducing
the need to prepare and plan a movement, but this
hypothesis requires further testing.
There is increasing attention for the possible beneficial
effects of physical exercise in Parkinson’s disease [77??].
Overall, physical functioning, balance, gait speed,
strength and health-related quality of life improve for
people with Parkinson’s disease after a physical exercise
intervention. Exercise therapy may also lead to a
Gait and balance in Parkinson’s disease Boonstra et al.
reduction in FOG . Management guidelines of the
American Academy for Neurology concluded that exer-
cise may be helpful in improving motor function in
people with Parkinson’s disease . However, there
exercise is beneficial for reducing falls or depression
[77??]. The lack of clear effect on falls was also shown
in an RCT, which showed that a combination of exercise
and movement strategies (i.e. prevention of falls and
movement initiation) only tended to decrease the inci-
dence of falls compared with controls receiving usual
care [80??]. However, it was encouraging that recurrent
near-falls were decreased in the intervention group, and
either with longer follow-up, a more intensive interven-
tion or prolonged treatment this may eventually translate
into fewer actual falls and injuries, possibly even among
Treadmill training may be one way to safely exercise
patients with Parkinson’s disease; for example, because
supervision is present or because a safety harness can
prevent actual falls. Several studies [81,82] have shown
that treadmill training can improve gait in Parkinson’s
disease. In addition, the Berg Balance Test, the Dynamic
Gait Index (a measure of gait adaptability) and FES
scores (a measure of balance confidence) improved
after 6 weeks of intensive treadmill training . An
alternative – and perhaps more enjoyable – way of
exercise training is dancing. One single-blind, small
sample RCT showed that tango dancing (20 sessions)
benefits patients with Parkinson’s disease, with improve-
ments in UPDRS, Berg Balance scale and a tendency for
less FOG .
A novel approach in delivering exercise is using motor
imagery, engaged previously to promote recovery of
stroke patients . An innovative study [85?] compared
a control group that was treated with physical exercise
alone with an experimental group that was treated with a
combination of actual physical exercise and imagery of
the very same exercises. The combined treatment group
showed the greatest improvement, but much work is
needed to fully underpin the merits of motor imagery
for rehabilitation in Parkinson’s disease.
A coincidental finding in two physiotherapy trials was the
problems encountered in finding and recruiting eligible
patients. In one UK-based study , only 13% out of all
patients listed in the clinical registers of Parkinson’s
disease specialists could be included in a falls prevention
trial, eligibility being the main problem. Similarly, a pilot
study based in the Netherlands was also troubled by
recruitment problems, but now mainly because most
patients in the Netherlands already receive physiother-
apy, so many declined the risk of being randomly allo-
cated to a ‘no physiotherapy’ control group . These
studies provide important lessons for future trials of
physiotherapy in Parkinson’s disease.
In 2007, evidence-based guidelines of physiotherapy for
Parkinson’s disease were published, including definitions
of the core treatment goals for physiotherapy (transfers,
capacity), as well as menus of treatment strategies tai-
lored to each of these domains [88?]. Specific recommen-
dations included: cueing strategies to improve gait; cog-
nitive movement strategies
exercises to improve balance; and training of joint mobi-
lity and muscle power to improve physical capacity.
to improve transfers;
The field of axial mobility deficits in Parkinson’s disease
continues to advance at a rapid pace, with significant
progress both at the fundamental level (improved
insights into the complex, multifactorial causes of falls,
gait and balance impairment) and at the clinical level
(with large scale trials now beginning to see the light).
Having said that, further work remains necessary to
design optimal treatment strategies and to adequately
prevent falls in Parkinson’s disease. Key targets for new
research include development of reliable and sensitive
outcome measures that are sufficiently feasible for wide-
spread application, in trials as well as everyday clinical
practice; and the development of improved treatment
strategies, including both pharmacotherapy (aimed at
more than just dopaminergic motor circuitries), stereo-
tactic surgery (optimizing STN stimulation and defining
new targets such as the PPN) and physiotherapy. A
particular challenge will be to combine these insights
into a comprehensive multifactorial approach aimed to
prevent falls, not only among those who have already
presented with falls, but also among prior nonfallers.
The present work was supported by NWO VIDI research grant
#016.076.352. The authors gratefully acknowledge the support of the
BrainGain Smart Mix Programme of the Netherlands Ministry of
Economic Affairs and the Netherlands Ministry of Education, Culture
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difficult itcan beto prevent fallsinParkinson’s disease, buthowdifficultitcan beto
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85 Download full-text
Tamir R, Dickstein R, Huberman M. Integration of motor imagery and physical
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Neurorehabil Neural Repair 2007; 21:68–75.
Preliminary, but innovative study that investigated the possible beneficial effect of
motor imagery as a tool for rehabilitation for patients with Parkinson’s disease. This
approach clearly deserves further study.
the databases of specialists in Parkinson’s disease. Parkinsonism Relat
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Evidence-based practice guidelines, detailing the core areas of physiotherapy for
Parkinson’s disease, and providing a menu of treatment strategies for each of
these domains. These guidelines are freely available via https://www.fysionet.nl/
Gait and balance in Parkinson’s disease Boonstra et al.