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Postural Instability in Patients With Parkinson's Disease

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postural instability in patients with parkinson disease, review from pubmed
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  REVIEW ARTICLE Postural Instability in Patients with Parkinson’s Disease Epidemiology, Pathophysiology and Management Samuel D. Kim  ã Natalie E. Allen  ã Colleen G. Canning  ã Victor S. C. Fung Published online: 18 October 2012   Springer International Publishing Switzerland 2012 Abstract  Postural instability is one of the cardinal signsin Parkinson’s disease (PD). It can be present even atdiagnosis, but becomes more prevalent and worsens withdisease progression. It represents one of the most disablingsymptoms in the advanced stages of the disease, as it isassociated with increased falls and loss of independence.Clinical and posturographic studies have contributed tosignificant advances in unravelling the complex patho-physiology of postural instability in patients with PD, but itstill remains yet to be fully clarified, partly due to thedifficulty in distinguishing between the disease process andthe compensatory mechanisms, but also due to the fact thatnon-standardized techniques are used to measure balanceand postural instability. There is increasing evidence thatphysical therapy, especially highly challenging balanceexercises, can improve postural stability and reduce the risk of falls, although the long-term effects of physical therapyinterventions on postural stability need to be exploredgiven the progressive nature of PD. Pharmacotherapy withdopaminergic medications can provide significantimprovements in postural instability in early- to mid-stagePD but the effects tend to wane with time consistent withspread of the disease process to non-dopaminergicpathways in advanced PD. Donepezil has been associatedwith a reduced risk of falls and methylphenidate has shownpotential benefit against freezing of gait, but the results areyet to be replicated in large randomized studies. Surgicaltreatments, including lesioning and deep brain stimulationsurgery targeting the subthalamic nucleus and the globuspallidus internus, tend to only provide modest benefitfor postural instability. New surgical targets such as thepedunculopontine nucleus have emerged as a potentialspecific therapy for postural instability and gait disorderbut remain experimental. 1 Introduction and Definition Posture and balance are the foundation on which uprightstance and walking are executed. The term ‘posture’describes the orientation of any body segment relative tothe gravitational vector and provides the mechanical sup-port for performing movements, while ‘balance’ is a gen-eric term describing the dynamics of body posture thatprevents falling in quiet stance or during locomotion [1, 2]. ‘Locomotion’, on the other hand, describes the forwardprogression associated with walking, and is criticallylinked with the ability to initiate and maintain rhythmicstepping [3]. Thus, postural and balance control can bedefined as stabilization or maintenance of ‘equilibrium’ of the body in relation to gravitational force under static anddynamic conditions, and ‘postural instability’, is theimpairment in balance that compromises the ability tomaintain or change posture such as standing and walking.Postural instability is considered to be one of the car-dinal features of Parkinson’s disease (PD) together withrest tremor, rigidity and bradykinesia [4]. It is present insome patients even at diagnosis and worsens with disease S. D. Kim    V. S. C. Fung ( & )Movement Disorders Unit, Department of Neurology, WestmeadHospital, Darcy Rd, Westmead, NSW 2145, Australiae-mail: vscfung@ozemail.com.auS. D. Kim    V. S. C. FungSydney Medical School-Western, The University of Sydney,Sydney, NSW, AustraliaN. E. Allen    C. G. CanningClinical and Rehabilitation Sciences Research Group,Faculty of Health Sciences, The University of Sydney,Sydney, NSW, AustraliaCNS Drugs (2013) 27:97–112DOI 10.1007/s40263-012-0012-3  progression, although when prominent early in the diseasecourse, it suggests the possibility of an atypical parkinso-nian disorder such as progressive supranuclear palsy ormultiple system atrophy [5].Postural instability is a major source of disability andreduced quality of life in PD [6]. In the DATATOP(Deprenyl And Tocopherol Antioxidative Therapy fOrParkinson’s disease) cohort, greater disability and moredepression were observed in PD patients with predominantpostural instability and gait disorder than those who hadtremor-dominant PD [7]. Furthermore, it not only corre-lates with falls [8] but also with fear of future falls, whichcan be incapacitating in its own right [9].Pathophysiology of postural instability is complex, withcontributions from the primary disease process and com-pensatory strategies. The most significant abnormality inpostural control results from impaired postural reflexeswith as yet incompletely understood mechanisms [10].This paper will review the epidemiology, pathophysiologyand, lastly, the management of postural instability in PD.As posture and balance are intimately related to walking,this paper will also briefly discuss the impact of posturalinstability on gait and falls. 2 Epidemiology 2.1 PrevalenceMild postural instability is reasonably common early inuntreated PD and seemingly inevitable in the later stages.Information from the Sydney multi-centre longitudinalstudy of PD shows that within 2 years of diagnosis, 34 %of the sample already demonstrated postural instability onthe basis of abnormal reactive postural responses, i.e.Hoehn and Yahr (H&Y) Stage 3 [11]. Ten years later,71 % of the surviving participants demonstrated posturalinstability, i.e. H&Y Stages 3–5 [12], while at the 15-yearfollow-up, postural instability was reported in 92 % of survivors [13]. At the 20-year follow-up, only one of thesurviving participants remained in H&Y Stage 2 [14]. Inaddition to abnormal postural responses, there is mountingevidence of abnormalities of anticipatory postural adjust-ments early in the disease process. In individuals in H&YStage 2, abnormal anticipatory postural adjustments duringturning have been reported [15], while abnormal sway instanding has been reported in recently diagnosed and un-medicated individuals [16]. Some postural instability in PDcould reasonably be attributed to the effects of ageing onsystems that contribute to postural stability. Nevertheless,studies that have compared people with PD with an age-matched control group consistently show people with PDhave greater deficits in postural stability [17–19] and higher fall rates [20–23]. In the largest prospective com- parative study to date [23], even those people with PD whodid not fall in the 12-month follow-up period had signifi-cantly poorer balance and gait scores than the healthy age-matched control group.In prospective studies, postural instability is consistentlyidentified as a risk factor for falls [24, 25]. Falls and recurrent falls occur at an alarmingly high rate in peoplewith PD. In a recent systematic review, 21 prospectivestudies reported the number of fallers and/or the number of falls in a sample of people with PD [26]. Between 35 and90 % of participants reported falling at least once duringmonitoring periods ranging from 3 months to over 2 years,while between 18 and 65 % of participants fell more thanonce. Furthermore, a meta-analysis of six prospectivestudies [27] shows that 21 % of people with PD who havenot fallen previously will fall within the next 3 months,indicating that prior falls is inadequate for predicting allfalls.In the USA (1999–2002), the direct annual healthcarecosts of PD was reported to be $US23,101 per person,which is double that of controls [28]. Although the impactof postural instability has not been specifically addressedfrom an economic perspective, increasing levels of motordisability have been reported to be associated withincreased healthcare and productivity costs [29].2.2 Impact of Postural Instability and Falls on Activityand ParticipationPostural instability and falls are significant causes of dis-ability, lost independence and reduced quality of life inpeople with PD [30–33]. The resulting pain [32], limitation of activities [20, 34, 35], fear of falling [9, 36] and unac- ceptably high levels of caregiver stress [37, 38] mean that the consequences of postural instability and falling aredevastating and widespread. A recent longitudinal studyshows that progression to H&Y Stage 3 is specificallyassociated with significant deterioration on quality of life[34]. However, even newly diagnosed individuals withpostural and gait instability experience more significantimpact on everyday activities and quality of life thanpatients with tremor-dominant symptoms [35]. As expec-ted, fear of falling is consistently reported to be associatedwith postural instability and falls [9, 39, 40]. However, there does appear to be a small subset of people with PD,who are highly unstable and fall frequently, while reportinglittle fear of falling [41]. Recent work also shows thatpeople with PD with postural and gait instability are morelikely to experience anxiety than those with tremor-domi-nant symptoms [42]. 98 S. D. Kim et al.  2.3 Risk Factors and Predictors of FallsDespite the high prevalence of postural instability and fallsin people with PD, the relationship between posturalinstability and falls is not entirely straightforward, withmany other risk factors for falls likely to act as modulators.A large number of risk factors for falls in people with PDhave been proposed in both prospective and retrospectivestudies, but they have not been consistently identifiedacross studies [21, 24, 25, 27, 43–46]. The two most comprehensive prospective studies [24, 25] both identified postural instability as an independent risk factor for falls.Latt and colleagues [25] have published the best prospec-tive explanatory model to date (sensitivity 77 %, specificity82 %) identifying freezing of gait (FOG), flexed posture,cognitive impairment, poor balance and leg weakness asindependent fall risk factors. Interestingly, although ageand co-morbidities such as postural hypotension and use of multiple medications were associated with falls in univar-iate models, these factors did not make a significant con-tribution to the multivariate model [25]. In addition, ameta-analysis of six prospective studies [27] indicates thatdisease severity is not a good predictor of falls, possiblybecause falls risk reduces with severe disease, which con-fines patients to a wheelchair or bed [20].The contribution of impaired cognition to falls has beenhighlighted in a recent prospective study of 164 individualswith PD [46]. Although specific measures of posturalinstability were not taken, fall frequency was analysed withrespect to cognition, disease severity, age, medications,orthostatic hypotension and visual impairment. In amultivariate model, adjusted for disease severity, fallfrequency was associated with power of attention andreaction time variability. Frontal cognitive impairment asassessed using the Frontal Assessment Battery [47] wasalso identified as an independent risk factor for falls [25],more so than low scores on the Mini-Mental State Exam-ination (MMSE) [48]. 3 Pathophysiology Postural and balance impairments are assessed eitherthrough quantitative laboratory-based systems or throughclinical observational tests. These studies have yieldedlimited and contradictory results, partly due to the fact thatthe PD population is diverse, but also because of the dif-ferences in study designs such as disease severity, defini-tion of fallers versus non-fallers and medication states, aswell as methods used to measure balance and posturalinstability [49]. The most significant insights have beengained from posturographic studies, using static andmoveable force platforms that measure the foot centre of pressure (COP) and other sway parameters under differenttreatment states, i.e. dopaminergic medications and/or deepbrain stimulation (DBS) surgeries. However, these studiesare beset by the fact that the techniques have not beenstandardized, making it difficult to interpret data obtainedacross different studies. In particular, studies under staticconditions have shown increased, normal [50] or evenreduced [51] spontaneous body sway, perhaps reflectingthe fact that reliability of postural sway can be influencedby disease and medication factors such as disabling dys-kinesia [52]. It is noteworthy that performance in some of these tests is only poorly related to clinical tests of balanceand history of falls [53]. In addition, the pull test, a com-monly used clinical test, is difficult to standardize and doesnot test anticipatory balance.3.1 Postural ReflexesMaintenance of an upright body posture in humans is anautomatic activity that requires minimal attention [17]. TheCNS provides coordination between posture, equilibriumand movement by utilizing two main mechanisms. Auto-matic postural reactions (APR) occur in response to sen-sory information, which signal postural disturbancescaused by movement, received from the visual, vestibularand somatosensory systems, while anticipatory posturaladjustments (APA) occur in association with voluntarymovements and dampen the effects of the forthcomingdisturbances by preceding the disturbance onset [54, 55]. Both anticipatory and reactive postural control mecha-nisms are altered in PD. Variable changes in APA havebeen reported, but this reflects the differences in the diseaseseverity of the study population. In early-stage PD patients,there is an exaggerated movement preparation when per-forming sit-to-stand tasks [56], while patients with moreadvanced disease tend to have reduced APAs [57], beingmore common in those with postural instability [58].Additionally, there is a variable pattern of muscle activa-tion [59] that does not correlate with bradykinesia, likelyreflecting deficits in the preparation and initiation of amotor act in PD.APR are also impaired in PD, with the early reactivetrunk movements being markedly reduced, and causing thetrunk to fall like a log in the direction of postural pertur-bation [60]. The postural reflexes show an abnormal patternof activation. The destabilizing medium-latency stretchreflexes are exaggerated, while the stabilizing long-latencystretch reflexes have been reported as either normal ordiminished [18, 60, 61]. Furthermore, the innervation sequence of long-latency reflexes is reversed in patientswith advanced disease [61]. Significantly, these reflexesadapt poorly to changes in postural tasks, e.g. PD patientshave impaired ability in suppressing postural responses in Postural Instability in Parkinson’s Disease 99  ankle muscles when the force platform perturbation sud-denly changes from backward translation to toes up rota-tion [62], and also display inadequate scaling of muscleactivation as well as impaired modification of the directionof ground reactive forces in response to changes in stancewidth [63, 64]. Moreover, PD patients have an impaired ability to suppress medium- and long-latency reflexes whenchanging from free stance to supported stance (holdingonto a stable structure) [50]. This impaired postural adap-tation to changes in postural tasks has been referred to as‘postural inflexibility’ [50, 51, 65]. There are variable reports of responsiveness of posturalinstability to levodopa, likely reflecting the differences inthe PD population studied as involvement of non-dopa-minergic systems becomes more important in advancedstages of the disease, especially with respect to gait andpostural control. Some have reported that there is nosignificant improvement or even worsening of posturalstability with levodopa, both clinically and as measured byincreased postural sway [7, 49], but others have contended that postural sway amplitude is only loosely related topostural stability [66], and there is good evidence that axialimpairments including postural instability and gait arelevodopa responsive, even in the advanced stages of thedisease, although these impairments are somewhat lessresponsive than bradykinesia and rigidity [67].A study [68] comparing the respective effects of levo-dopa and subthalamic nucleus-DBS (STN-DBS) on pos-tural stability in advanced PD patients (mean H&Y Stage 3off therapy; mean disease duration 12.9 years) has dem-onstrated that levodopa therapy provides a similar magni-tude of benefit in clinical measures as measured by theUnified Parkinson’s Disease Rating Scale (UPDRS) [69]compared with ‘off’ states, although objective measures(posturography) reveal a greater magnitude of benefit withSTN-DBS [68]. In this study, PD patients had abnormalposterior displacement of foot COP and levodopa restoreda forward position in both static and dynamic conditions.Similar posturographic results were reported by Bloemet al. [70], although they only reported partial improvementin COP displacement, and there was a failure of correctionof medium-latency reflex amplitudes. 3.1.1 What Underlies Impaired Postural Reflexes? It has been hypothesized that disordered basal gangliaphysiology and dopaminergic deficit underlie the derangedpostural reflexes in PD. Specifically, increased medium-latency reflex amplitude results from reduced inhibitoryoutput of the nigrostriatal circuit due to dopaminergicdeficit while reversed long-latency reflex innervationsequence reflects failure of selection and initiation of appropriate motor programmes in PD [18, 71–73]. Furthermore, dopaminergic deficit correlates with thedegree of impairment of stabilizing long-latency reflexes.Patients with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced parkinsonism have greatest impairment instabilizing long-latency postural reflexes, followed in orderby young PD patients, those exposed to neuroleptic with orwithout extrapyramidal symptoms, and normal controls,suggesting that long-latency reflexes are under supraspinaldopaminergic control [74].In support of the role of basal ganglia in posturalinstability, studies of ground reactive forces with moveableforce platforms have revealed that PD patients have largerthan normal passive reactive forces and smaller than nor-mal reactive forces in the active period, consistent withparkinsonian rigidity and bradykinesia, respectively [19].In line with this, PD patients when falling tend to fall like alog, with smaller hip and knee displacements and excessiveco-contraction of antagonistic hip and trunk muscles,consistent with the anticipated effects of truncal rigidity[60]. However, the abnormal direction and inflexibility of reactive forces (i.e. impaired postural reflexes) cannot beexplained solely on the basis of rigidity and bradykinesia,suggesting additional deficits in APR [64]. Postural defi-cits, at least in more severe disease, tend to be levodoparesistant [19, 75], and the fact that levodopa has no sig- nificant effect on axial tone, suggests that axial andappendicular tone are controlled by different circuits [76].Furthermore, nigral cell loss, as documented with fluo-rodopa positron emission tomography (PET) scans, showsan excellent correlation with bradykinesia, but much less sowith postural instability [77]. It is of potential relevancethat truncal rigidity can be a compensatory strategy inresponse to fear of falls, as a stiffening strategy, whichreduces the degree of freedom of movement and simplifiespostural control. This strategy is seen in healthy controlswhen made artificially fearful by standing on an elevatedplatform [78, 79]. Disentangling pathological from compensatory truncal stiffness in PD patients remains achallenge.3.2 Effects of Stooped Posture on Postural ControlIn PD patients, there appears to be an excessive forwardshift in foot COP, which correlates with disease severity asmeasured by the motor section of the UPDRS. However,conflicting results have also been reported, includingreports of no significant change in foot COP [80], as well asa variable change in foot COP depending on diseaseseverity, with a backward shift in the less affected and aforward shift in more affected patients [50].Although stooped posture has been identified as anindependent risk factor for falls in PD [25], this posture andchanges in foot COP may be compensatory [81, 82]. First, 100 S. D. Kim et al.
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