Introduction 11 Anup

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Effect of walking along circle on foot prints in

Parkinsons on Freezing

INTRODUCTION

Parkinsonism disease is named after the English doctor James Parkinson,

who published the first detailed description in An Essay on the Shaking Palsy in

1817.

Parkinsons disease (PD) is chronic progressive disease of nervous

system by the cardinal features of Rigidity, Akinesia, Bradykinesia, Tremors and

Postural Instability. In addition the disease may cause variety of indirectimpairments and complications of the cardinal including, movement and gait

disturbances, masked face, cognitive and perceptual communication and

swallowing dysfunction and autonomic dysfunction1.

EPIDEMIOLOGY & INCIDENCE

Parkinsons disease is the second most common neurodegenerative

disorder after Alzheimer's disease.2 The prevalence of Parkinsons disease is

about 0.3% of the whole population in industrialized countries. Parkinsons

disease is more common in the elderly and prevalence rises from 1% in those

over 60 years of age to 4% of the population over 802. The mean age of onset is

around 60 years, although 510% of cases, classified as young onset, begin

between the ages of 20 and 50.2 Parkinsons disease may be less prevalent in

those of African and Asian ancestry, although this finding is disputed.2 Some

studies have proposed that it is more common in men than women, but others

failed to detect any differences between the two sexes2. The incidence of

Parkinsons disease is between 8 and 18 per 100,000 person years.2In United

States there are 1.5 million individuals with Parkinsons disease with 50,000 new

cases appearing annually. The mean onset is between 58 and 62 years with
http://en.wikipedia.org/wiki/James_Parkinsonhttp://en.wikipedia.org/wiki/Neurodegenerationhttp://en.wikipedia.org/wiki/Neurodegenerationhttp://en.wikipedia.org/wiki/Alzheimer%27s_diseasehttp://en.wikipedia.org/wiki/Alzheimer%27s_diseasehttp://en.wikipedia.org/wiki/Prevalencehttp://en.wikipedia.org/wiki/Incidence_%28epidemiology%29http://en.wikipedia.org/wiki/Incidence_%28epidemiology%29http://en.wikipedia.org/wiki/Prevalencehttp://en.wikipedia.org/wiki/Alzheimer%27s_diseasehttp://en.wikipedia.org/wiki/Neurodegenerationhttp://en.wikipedia.org/wiki/Neurodegenerationhttp://en.wikipedia.org/wiki/James_Parkinson


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majority of cases having their onset between 50 and 79 years. A small

percentage as many as 10 percent develops young onsets Parkinsons disease,

which is defined by the appearance of initial symptoms before age of 40.

Individuals usually have more benign long-term course1.

PARKINSON-PLUS SYNDROMES

Parkinson-plus syndromes also known as disorders of multiple systemdegeneration, are a group of neurodegenerative diseases featuring the classical

features of Parkinson's disease having cardinal features Tremor, Rrigidity,

Akinesia/ Bradykinesia, Postural instability with additional features that

distinguish them from simple idiopathic Parkinson's disease. Some consider

Alzheimer's disease to be in this group. The atypical Parkinsonian or Parkinson

Plus syndromes are often difficult to differentiate from Parkinson's disease and

each other. They include multiple system atrophy (MSA), progressive

supranuclear palsy (PSP), and corticobasal degeneration (CBGD). Dementia

with Lewy bodies (DLB), may or may not be part of the PD spectrum, but it is

increasingly recognized as the second most common type of neurodegenerative

dementia after Alzheimer's disease..Additional Parkinson-plus syndromes include

Pick's disease and olivopontocerebellar atrophy (OPCA). The latter is

characterized by Ataxia and Dysarthria, and may occur either as an inherited

disorder or as a variant of multiple system atrophy. Multiple system atrophy is

also characterized by autonomic failure, formerly known as Shy-Drager

syndrome1.

ETIOLOGY

The etiology of Parkinsons disease remains unknown and the consensus

is that it is multifactorial. A slow viral processes or long term effects of early

infection were implicated in post-encephalitis Parkinsonism. Some evidence

show that environmental factors are involved in the cause and that the interaction
http://en.wikipedia.org/wiki/Parkinson%27s_diseasehttp://en.wikipedia.org/wiki/Parkinson%27s_diseasehttp://en.wikipedia.org/wiki/Tremorhttp://en.wikipedia.org/wiki/Rigidityhttp://en.wikipedia.org/wiki/Akinesiahttp://en.wikipedia.org/wiki/Bradykinesiahttp://en.wikipedia.org/wiki/Postural_instabilityhttp://en.wikipedia.org/wiki/Idiopathichttp://en.wikipedia.org/wiki/Alzheimer%27s_diseasehttp://en.wikipedia.org/wiki/Multiple_system_atrophyhttp://en.wikipedia.org/wiki/Progressive_supranuclear_palsyhttp://en.wikipedia.org/wiki/Progressive_supranuclear_palsyhttp://en.wikipedia.org/wiki/Corticobasal_degenerationhttp://en.wikipedia.org/wiki/Dementia_with_Lewy_bodieshttp://en.wikipedia.org/wiki/Dementia_with_Lewy_bodieshttp://en.wikipedia.org/wiki/Pick%27s_diseasehttp://en.wikipedia.org/wiki/Olivopontocerebellar_atrophyhttp://en.wikipedia.org/wiki/Ataxiahttp://en.wikipedia.org/wiki/Dysarthriahttp://en.wikipedia.org/wiki/Autonomichttp://en.wikipedia.org/wiki/Shy-Drager_syndromehttp://en.wikipedia.org/wiki/Shy-Drager_syndromehttp://en.wikipedia.org/wiki/Shy-Drager_syndromehttp://en.wikipedia.org/wiki/Shy-Drager_syndromehttp://en.wikipedia.org/wiki/Shy-Drager_syndromehttp://en.wikipedia.org/wiki/Autonomichttp://en.wikipedia.org/wiki/Dysarthriahttp://en.wikipedia.org/wiki/Ataxiahttp://en.wikipedia.org/wiki/Olivopontocerebellar_atrophyhttp://en.wikipedia.org/wiki/Pick%27s_diseasehttp://en.wikipedia.org/wiki/Dementia_with_Lewy_bodieshttp://en.wikipedia.org/wiki/Dementia_with_Lewy_bodieshttp://en.wikipedia.org/wiki/Corticobasal_degenerationhttp://en.wikipedia.org/wiki/Progressive_supranuclear_palsyhttp://en.wikipedia.org/wiki/Progressive_supranuclear_palsyhttp://en.wikipedia.org/wiki/Multiple_system_atrophyhttp://en.wikipedia.org/wiki/Alzheimer%27s_diseasehttp://en.wikipedia.org/wiki/Idiopathichttp://en.wikipedia.org/wiki/Postural_instabilityhttp://en.wikipedia.org/wiki/Bradykinesiahttp://en.wikipedia.org/wiki/Akinesiahttp://en.wikipedia.org/wiki/Rigidityhttp://en.wikipedia.org/wiki/Tremorhttp://en.wikipedia.org/wiki/Parkinson%27s_disease


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of the environment and ageing lead to a critical decrease in dopamine. Several

investigators have found a link between growing up in a rural areas and

Parkinsons disease; the important factor includes pesticides use, insecticides

use and well water. The accumulation of free radicals cell death from toxins to

the excitatory neurons, and dysfunction of nigral mitochondria have been

implicated in pathological process. Genetics may also be a factor in Parkinson

disease1.

The term Parkinsonism is used to refer to a group of disorder that produce

abnormalities of basal ganglia function. Parkinsons disease or primary

Parkinsonism is the most conditions common cause affecting approximately 78%

of patients. Secondary Parkinsonism results from a number of different causes,

including inherited & acquired neurodegenerative disorders. The term

Parkinsonism plus syndromes refer to those conditions with the symptoms of

multiple system degeneration1.

Parkinsons disease (primary Parkinsonism): Etiology is idiopathic or

unknown. Two distinct clinical subgroups have been identified, one group

includes individuals whose dominant symptoms include postural instability & gait

disturbances, (PIGD) another group includes individuals with tremors as themain feature & demonstrate few problems with Bradykinesia and Postural

Instability1.

Post Infectious Parkinsonism (Secondary Parkinsonism): The

development of Parkinsonism with other encephalitic conditions is rare. The

onset of the symptoms typically occurred after many years, giving rise to the

theory that a slow virus was affecting the brain there has been no recurrence of

this influenza and incidence is slowly decreasing in frequency.

Toxic Parkinsonism:Parkinsons symptoms occur in individual exposed to

certain industrial poisons and chemicals like Manganese, Carbon disulfide,

Carbon Monoxide, Cyanide, and Methanol the most common of these toxins is


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manganese, which represents serious occupational hazards to many miners.

Severe and lasting classic Parkinsons has been inadvertently produced in

individuals who injected a synthetic heroin containing the chemical Methyl phenyl

tetrahydropyridin1

Drug-Induced Parkinsonism: A variety of drug can produce extra

pyramidal dysfunction that mimics the sign of Parkinsons disease. These drugs

are thought to interfere with dopaminergic mechanisms either presynaptically or

postsynaptically they include

1. Neuroleptic-drugs such as chlorpromazine (thorazine), haloperidol (haldol),

thioridazine and thiothexine(navane);

2. Antidepressant drugs such as amitriptyline(triavil), amoxapine(Asendin),&

trazodone (Desyrel).

3. Antihypertensive drugs such as methylodopaand reserpine.high doses of

these drugs are problematic in elderly.

Withdrawal of these agents usually reverses the symptoms within few weeks,

although in some cases the effects can persist and may be related to subclinical

Parkinsons disease.

Metabolic causes: Parkinsonism can cause in rare cases by metabolic

conditions, including the disorders of calcium metabolism that result in BG

calcifications. These include hypothyroidism, hyperparathyroidism,

hypoparathyroidism and Wilsons disease1.


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PATHOPHYSIOLOGY

The term Parkinsons used to refer to a group of disorders that produce

abnormalities of basal ganglia function. The basal ganglia are collection of inter

connected grey matter nuclear masses deep within the brain. It is now

considered to be composed of the caudate and putamen (collectively term as

straitum) plus the globus pallidus, subthalamic nucleus and substantia nigra. The

basal ganglion plays an important role in production of voluntary movements and

control of postural adjustments associated with voluntary movements. Activity is

initiated by input to the main input nuclei, caudate and putamen, from cerebral

cortex and thalamus. Widespread cortical areas are involved in sending signals

to basal ganglia, including sensory, motor and associated areas. The striatum

also receives input from substantia nigra and pedunculopontine tegmental

nucleus of midbrain. Output is channeled primarily through gobus pallidus and

substantia nigra via thalamocortical projections to frontal and premotor cortex

areas. Within the Basal ganglion, information is integrated and modulated from

cerebral cortex and thalamus through multiple parallel circuits. These complexcircuits are divided into direct and indirect anatomical pathways have opposing

actions. The direct pathways that have facilitates flow to thalamus activating

some movements while indirect pathways inhibits information flow and suppress

movements.

Damage to the Basal Ganglion results in motor disturbances that can be

hyperkinetic or hypokinetic. Hyperkinetic disturbances are characterized by

excessive or abnormal movements. Hypokinetic disturbances are characterized

by slowness or lack of movement. The substentia nigra, pars compcta works to

facilitate movement through both direct and indirect pathways of motor loop 1.

Parkinsons disease is associated with dopaminergic neuron that

produces dopamine. They have they have their cell bodies in substantia nigra


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pars compacta and send their axons to straitum i.e. caudate nucleus and

putamen. A degeneration of 80% of neuron is estimated to occur before signs of

disease became clinically evident. Nigral cell loss is more prevalent in ventral cell

group and loss of melanin containing neurons produces characteristic changes in

depigmentation. There are other deficiencies as well (e.g. Serotonin,

norepinephrin). As disease progresses and neuron degenerates, they develop

characteristic cytoplasmic inclusion bodies, called Lewys bodies1. Other sites of

predilection include the dorsal motor nucleus of the vagus, the hypothalamus, the

locus ceruleus, the cerebral cortex and the autonomic ganglia4, 5, 6.


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Fig 1: Schematic diagram of the direct (Dir.) and indirect (Indir.) pathways

of the basal ganglia motor circuits in normal and parkinsonian states

Loss of dopaminergic neuron influence leads to a reduction in

spontaneous movement. Thus the patient wants to move but cannot. Tremors

and rigidity are viewed as re release phenomenon, represents of loss of inhibitory

influences BG. Significant changes in straital dopamine receptors also occurs,

resulting in decreased binding for dopamine in the BG. This may explain loss of

clinical effectiveness of l-dopa. During later stages of disease7, 8,9.

Dig 2: showing Typical Parkinsons Features


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BRADYKINESIA

Bradykinesia, or slowness of movement, is often used interchangeably

with hypokinesia (poverty of movement) and akinesia (absence of movement).

Bradykinesia is the most characteristic symptom of basal ganglia dysfunction in

PD10. It may be manifested by a delay in the initiation and slowness of execution

of a movement. Other aspects of bradykinesia include a delay in arresting

movement, decrementing amplitude and speed of repetitive movement, and an

inability to execute simultaneous or sequential actions.

TREMOR

Tremor, although less specific than bradykinesia, is one of the most

recognizable symptoms of Parkinson s disease. However, only half of all

patients present with tremor as the initial manifestation of Parkinsons disease,

and 15% never have tremor11. Although tremor at rest (46 Hz) is the typical

Parkinsonian tremor, most patients also have tremor during activity, and this

postural tremor (58 Hz) may be more disabling than the resting tremor. Postural

tremor without Parkinsonian features and without any other known etiology is

often diagnosed as essential tremor (ET).

RIGIDITY

Rigidity is less variable than tremor, and it probably better reflects the

patients functional disability. Rigidity may contribute to subjective stiffness and

tightness, a common complaint in patients with PD. However, there is relatively

poor correlation between the sensory complaints experienced by most patients

and the degree of rigidity12,13. Rigidity is often associated with postural deformity,


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resulting in flexed neck and trunk posture and flexed elbows and knees. Some

patients develop ulnar deviation of hands (striatal hand), which can be confused

with arthritis14,15

LOSS OF BALANCE

The loss of balance associated with propulsion and retropulsion is

probably the least specific, but most disabling, of all parkinsonian symptoms.

Loss of postural reflexes usually occurs in more advanced stages of PD and,

along with freezing, is the most common cause of falls, often resulting in hip

fractures. The loss of protective reactions further contributes to fall-related

injuries. Many patients with postural instability, particularly when associated with

flexed trunkal posture, have festination, manifested by faster and faster walking

in order to prevent falling. When combined with axial rigidity and bradykinesia,

loss of postural reflexes causes the patient to collapse into the chair when

attempting to sit down. The pull test (pulling the patient by the shoulders) is

commonly used to determine the degree of retropulsion or propulsion.

GAIT AND POSTURAL PROBLEMS

The gait and postural problems associated with PD probably result from a

combination of bradykinesia, rigidity, loss of anticipatory proprioceptive reflexes,

loss of protective reaction to a fall, gait and axial apraxia, ataxia, vestibular

dysfunction, and orthostatic hypotension. When gait disorder, with or without

freezing and posturalinstability, is the dominant motor dysfunction, lower body

parkinsonism should be considered in the differential diagnosis16. This syndrome

is thought to represent a form of vascular parkinsonism associated with a multi-

infarct state. Furthermore, gait disorder and postural instability are typically

associated with PSP17, 18.


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FREEZING

One of the most disabling symptoms of Parkinsons disease is freezing ormotor blocks, a form of akinesia19, 20. The observation that some patients even

with severe bradykinesia have no freezing and other patients have a great deal

of freezing but minimal or no bradykinesia suggests that the two signs have

different pathophysiologies. Furthermore, that bradykinesia usually responds well

to levodopa and freezing does not indicates that freezing may be a manifestation

of a nondopaminergic disturbance. Freezing consists of a sudden, transient (a

few seconds) inability to move. It typically causes start hesitation when initiating

walking and the sudden inability to move the feet (as if glued to the ground)

when turning or walking through narrow passages (such as the door or the

elevator), when crossing streets with heavy traffic, or when approaching a

destination (target hesitation). Patients often learn a variety of tricks to overcome

freezing, such as marching to command (left, right, left, right), visual cues such

as stepping over objects (end of a walking stick, pavement stone, cracks in the

floor, etc.), walking to music or metronome, shifting body weight, rocking

movements, and others16, 21, 22. When freezing occurs early in the course of the

disease or is the predominant symptom, a diagnosis other than PD should be

considered.

Many individuals with Parkinson disease (PD) experience difficulty turning

and freezing of gait that can lead to falls. Falls during turning are eight times

more likely to result in hip fracture than falls during straight walking23 and

individuals with PD are 3.2 times more likely to sustain a hip fracture than people

of similar age without PD

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. Given the substantial personal and financial costsassociated with this problem, it is clear that strategies are needed to address

turning difficulties in order to reduce falls and fractures.

The underlying impairments that lead to freezing have not been clearly

identified but several theories exist. One proposition is that freezing results from

a combination of hypokinesia and the sequence effect25. Hypokinesia refers to


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the fact that steps are smaller than normal at the outset of walking and the

sequence effect refers to the fact that steps become progressively smaller over

the course of a walking trial. Interventions to enhance either baseline step size or

to maintain the step size across a trial could both contribute to a reduction of

freezing.

Freezing of gait is also associated with gait asymmetry26. Individuals with

freezing of gait have asymmetrical swing times. Turns are inherently

asymmetrical, with the outer limb traveling further than the inner limb. As such,

baseline gait asymmetries may be more problematic during turning than during

straight walking. The asymmetrical nature of turns may contribute to turns being

a major trigger for freezing. Though never studied, it may be that individuals with

more pronounced gait asymmetry are the ones who have difficulty turning and

that turns are most difficult when the limb that normally has the shorter swing

time is required to be the outer limb, i.e. the limb that now needs to have a longer

swing time. If overcoming baseline asymmetry when turning toward the limb that

normally has the longer swing time is problematic, then training to counteract the

baseline asymmetry and facilitate turning in this direction could be useful.

Yet another possible mechanism for freezing is difficulty switching

between motor tasks27.Perhaps turning triggers freezing because the transition

from straight walking to a turning pattern is impaired in PD. Multiple studies have

demonstrated that subjects with PD have difficulty with internally cued

movements, but often respond well to external cues28. The Walking on circle on

foot prints could serve as an external cue for turning. Through practice of

externally cued turning, a motor pattern appropriate for turning may become

more automatic, facilitating the ease of switching between straight walking and

turning.


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NEED FOR STUDY

One of the most disabling symptoms of Parkinsons disease is freezing.The underlying impairments that lead to freezing have not been clearly identified.

Freezing of gait that can lead to falls and also risk increases 8 times while

turning. There is impaired internal clueing in Parkinsons patient. Hence giving

external clueing as foot prints and repeated turning like making them to walk on

circle we are trying to reduce freezing.


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HYPOTHESIS

NULL HYPOTHESIS

Walking along the circle on foot prints does not show any effect in

Parkinsons on freezing.

ALTERNATIVE HYPOTHESIS

1. Walking along the circle on foot prints reduces freezing in Parkinsons.

2. Walking along the circle on foot prints increases freezing in Parkinsons.


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AIM & OBJECTIVES

AIM:

To study effect of walking along the circle on foot prints in Parkinsons on

freezing.

OBJECTIVES:

1. To evaluate the efficacy of walking along the the circle on foot prints on

freezing in Parkinsons patients.

2. To confirm if walking and continues turning is effective in Parkinsons

patient.


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REVIEW OF LITERATURE

Melton LJ 3rd et al (2006) Using the data resources of the Rochester

Epidemiology Project, information about PD, dementia, other clinical risk factors

for fracture and fracture events was obtained from review of complete inpatient

and outpatient medical records spanning each subject's residence in the

community. Compared to an equal number of age- and sex-matched non-PD

referent subjects from the community, PD patients were at a 2.2-fold increased

risk of fractures generally and a 3.2-fold greater risk of hip fractures specifically.

Adjusting for age, the independent predictors of overall fracture risk in the PD

subjects included female sex (hazard ratio [HR] 1.6; 95% confidence interval [CI],

1.1-2.3), dementia (HR, 1.6; 95% CI, 1.1-2.4) and chronic depression, which was

associated with a reduced risk (HR, 0.4; 95% CI, 0.2-0.8). Hip fractures were

predicted by dementia (HR, 2.2; 95% CI, 1.2-4.1). The increased fracture risk in

patients with PD is not entirely explained by concomitant dementia, andadditional study is needed to determine the relative contributions to fracture risk

of falls versus bone loss in these patients.

Stack EL et al(2006) Difficulty turning (DT) is common in Parkinson's disease

(PD). We set out to answer the questions. 75 people (median age 75 years; PDduration 7 years) answered questions about DT, freezing and falls and

completed a standard 180 degrees turn test and an everyday task necessitating

spontaneous turns, later rated from video by blinded assessors. Forty-two people

reported DT, of whom 86% reported frequent freezing and/or falls. Twenty-six

people with DT and 15 without completed the functional task. Greater proportions


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of the former appeared Unstable (12 vs 1; P = 0.014), lacked Heel Strike (25 vs

9; P = 0.006) and Used Support (7 vs 0; P = 0.035): the former took more

Turning Steps (medians 6 vs 4; P = 0.001). The 95% limits of agreement

between step counts (functional vs standard turns) ran from -6.3 to 3.6 steps. Of

49 people with a history of freezing and/or falls, 36 (73%) reported frequent

DT.People who report DT turn differently to those who report no problems.

Standard turn tests poorly reflect step count during real-life turning, whereas

unobtrusive structured observation reveals the turning strategies people use, so

can guide rehabilitation. Reported DT is a sensitive indicator of freezing and/or

falling, both indicators for physiotherapy.

Iansek R et al (2006) Festination and freezing of gait (FOG) are poorly

understood gait disorders that cause disability and falls in people with Parkinson

disease (PD). In PD, basal ganglia malfunction leads to motor set deficits

(hypokinesia), while altered motor cue production leads to a sequence effect,

whereby movements becomes progressively smaller as in festination. We

suggest both factors may contribute to FOG. Disturbance of set maintenance by

the basal ganglia in PD has previously been examined in gait, but limited

systematic evaluation of the sequence effect exists. In this study, we investigated

the step-to-step amplitude relationship in 10 PD subjects with clinical evidence of

festination and FOG. Four conditions were examined: off levodopa, off with

attentional strategies, off with visual cues, and on levodopa. Participants

demonstrated a sequence effect (F = 6.24; P = 0.001), which was reversed only

by use of visual cues. In contrast, medication, attentional strategies, and visual

cues all improved hypokinesia. Variability was marked both within and between

participants in all conditions. The variability of FOG is suggested to relate to a

combination of factors, including the sequence effect and its variability, as well as

the severity of hypokinesia and its response to medications.


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A Nieuwboer et al (2007) Gait and mobility problems are difficult to treat in

people with Parkinsons disease. The Rehabilitation in Parkinsons Disease:

Strategies for Cueing (RESCUE) trial investigated the effects of a home

physiotherapy programme based on rhythmical cueing on gait and gait-related

activity. A single-blind randomised crossover trial was set up, including 153

patients with Parkinsons disease aged between 41 and 80 years and in Hoehn

and Yahr stage IIIV. Subjects allocated to early intervention (n = 76) received a

3-week home cueing programme using a prototype cueing device, followed by 3

weeks without training. Patients allocated to late intervention (n = 77) underwent

the same intervention and control period in reverse order. After the initial 6

weeks, both groups had a 6-week follow-up without training. Posture and gait

scores (PG scores) measured at 3, 6 and 12 weeks by blinded testers were the

primary outcome measure. Secondary outcomes included specific measures on

gait, freezing and balance, functional activities, quality of life and carer strain.

Small but significant improvements were found after intervention of 4.2% on the

PG scores (p = 0.005). Severity of freezing was reduced by 5.5% in freezers only

(p = 0.007). Gait speed (p = 0.005), step length (p,0.001) and timed balance tests

(p = 0.003) improved in the full cohort. Other than a greater confidence to carryout functional activities (Falls Efficacy Scale, p = 0.04), no carry-over effects were

observed in functional and quality of life domains. Effects of intervention had

reduced considerably at 6-week follow-up. Cueing training in the home has

specific effects on gait, freezing and balance. The decline in

effectiveness of intervention effects underscores the need for permanent cueing

devices and follow-up treatment. Cueing training may be a useful therapeutic

adjunct to the overall management of gait disturbance in Parkinsons disease.

Q J Almeida, C A Lebold (2009) While freezing of gait (FOG) is typically

considered a motor impairment, the fact that it occurs more frequently in confined

spaces suggests that perception of space might contribute to FOG. The present


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study evaluated how doorway size influenced characteristics of gait that might be

indicative of freezing. Changes in spatiotemporal aspects of gait were evaluated

while walking through three different-sized doorways (narrow (0.675 m wide 3 2.1

m high), normal (0.9 m wide 32.1 m high) and wide (1.8 m wide 3 2.1 m high)) in

three separate groups: 15 individuals with Parkinsons disease confirmed to be

experiencing FOG at the time of test; 16 non-FOG individuals with Parkinsons

disease and 16 healthy age-matched control participants. Results for step length

indicated that the FOG group was most affected by the narrow doorway and was

the only group whose step length was dependent on upcoming doorway size as

indicated by a significant interaction of group by condition (F(4,88)2.73,

p


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more frequently if a significant sequence effect (measured as a regression slope)

was co-existent in the subject. Twenty-six participants with Parkinsons disease

were separated clinically into a freezing (PD + FOG, n = 16) and non-freezing

(PD FOG,

n = 10) group, with 10 age-matched control participants. Testing involved walking

trials where preferred step length was set at 100%, 75%, 50% and 25% of

normalized step length. The number of FOG episodes increased in the 50%

condition and further

increased in the 25% condition compared to other conditions. The participants

with FOG also demonstrated a larger average regression slope, with significant

differences in the 75%, 50% and 25% conditions when compared to the PD FOG

and control groups. There were no significant differences when comparing the

slope of the PD FOG and control group, indicating the reduced step length and

the sequence effect may have led to the occurrence of FOG. These findings

support the possible dual requirement of a reduced step length and a successive

step to step amplitude reduction to lead to FOG.

Yohei Okada et al (2011) The purpose of this study was to investigate

abnormalities of the first three steps of gait initiation in patients with Parkinsons

disease (PD) with freezing of gait (FOG). Ten PDpatients with FOG and 10 age-

matched healthy controls performed self-generated gait initiation. The center of

pressure (COP), heel contact positions, and spatiotemporal parameters were

estimated from the vertical pressures on the surface of the force platform. The

initial swing side of gait initiation was consistent among the trials in healthy

controls but not among the trials in PD patients. The COP and the heel contact

position deviated to the initial swing side during the first step, and the COP

passed medial to each heel contact position during the first two steps in PD

patients. Medial deviation of the COP fromthe first heel contact position had

significant correlation with FOG questionnaire item5. These findings indicate that

weight shifting between the legs is abnormal and thatmedial deviation of the COP


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from the first heel contact position sensitively reflects the severity of FOG during

the first three steps of gait initiation in PD patients with FOG.

Quincy J. Et al (2011) Visual cues are known to improve gait in Parkinsons

disease (PD); however, the contribution of optic flow continues to be disputed.

This study manipulated transverse line cues during two gait training interventions

(6 weeks). PD subjects (N =42) were assigned to one of three groups: treadmill

(TG), overground (OG), or control group (CG). Participants walked across lines

placed on either treadmills or 16-meter carpets, respectively. The treadmill (TG)

offered a reduced dynamic flow from the environment, while lines presented on

the ground (OG) emphasized optic flow related to the participants own

displacement. Both interventions significantly improved (andmaintained through

retention period) step length, thus improving walking velocity.Only the OG

improved in the TUG test, while only the TG showed hints of improving (and

maintaining) motor symptoms. Since gait improvements were found in both

training groups, we conclude that by reducing optic flow, gait benefits associated

with visual cueing training can still be achieved.


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MATERIALS & METHODOLOGY

STUDY DESIGN : Experimental study

STUDY SETTING : At the nearby health care institution approved

by the guide & college

TARGET POPULATION : Patients Diagnosed as Parkinsons on Hoen

And

Yahr stage 1-4.

SAMPLE POPULATION : Subjects with Freezing

SAMPLING METHOD : Simple random

SAMPLE SIZE : 30

SAMPLE DESIGN : Purposive

INCLUSION CRITERIA:

1. Patients scored between stage 1-4 on Hoen and Yahr scale.

2. Patients having episodes of freezing during turning activity.

3. Both male and female patients of Parkinsons disease.

4. Patients of age group from 50 to 80 years

EXCLUSION CRITERIA:

1. Patients who are having visual, auditory and sensory deficits

2. Patients who are unable to stand

3. Having cardio repiratory prob, stroke or dyspnea.

4. Patients who walks with the help of walking aids.


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MATERIALS REQUIRED Ink

Stop watch Inch tape

Hoen and yahr Scale

OUTCOME MEASURES

Gait parameters like:

Stride length : The linear distance between two successive point of contact of

same lower extremity.

Step length : The linear distance between two successive point of contact of

opposite extremity.

Freezing : The number of time subject got freeze while walking on zigzag

lines.

episodes

Time taken : The time taken to resolve the freezing noted before and after

to resolve


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METHODOLOGY

A list of subjects of Parkinsons patient was obtained from Parkinsons

Association. Subjects having freezing selected on the basis of inclusion criteria.

Out of these short listed individuals, 30 subjects were selected by random

sampling for the actual study. Oral information was given to all the subjects about

this study and also the importance of this study was explained in detail to them.

Written consent was taken from all the samples included in this study. Also a

written permission was taken from the Head of Parkinsons Association for

introducing and allowing to include there members in the study.

The subjects asked to walk along the circle having foot prints on it. First

the subjects were asked to walk along the straight line with distance of 5 meters

having ink on their foot so as to calculate the step length and stride length of that

person. Ink was applied with the help of brush and in between two times again

the same procedure is perform. The readings has been noted before the

protocol. Also the subjects were asked to walk along the zigzag lines each line

is making angle of 45 degrees with each other and number of time subject got

freeze and time taken to resolve the freezing noted before and after protocol.

Subjects were asked to walk on circle having foot prints printed on it for six

weeks and 5 days a week. Total of 30 sessions were given. After that post

protocol readings are noted on 30th session.


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Description

Walk on straight line as normally as everyday subject does.

Concentrate on walking and do not have any other thoughts.

Try and make surroundings as sound as possible.

Walk on zig zag lines.

Walk on circle keep your foot exactly on foot prints on circle.

Walk in clockwise and anticlockwise direction.

Stop if overexertion happens.


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DATA RECORDING AND ANALYSIS

DATA RECORDING

Gait parameter is documented prior to the study and after 6 weeks protocol by

taking footprints

Also freezing episodes and time taken to resolve documented.

DATA ANALYSIS

It is done by using paired t-test.


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STAISTICAL ANALYSIS

The statistical tests used for the analysis of the result:

1) Paired t-test

Mean, standard deviation and standard error was carried out for all the

groups. In this table following statistical formulae have been used for analysis:

Formula

1. Mean X = X / n

Where X is a given variable

n is total number of subjects

Standard Deviation = )( XX2

n-1

Where X = Individual Score

X = The Mean Score

N = Total number of Subjects


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PAIRED t TEST =

d

t =

n d2 - ( d)

2

n 1

Where; d = difference between each subject pair of scores

d = the total of the differences

( d)2 = the total of the differences, squared.

d2 = the total of the squared differences.

n = number of subjects, or pairs of matched subjects.


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DATA ANALYSIS

Graph 1

Number male and female out of total number of subjects

Table 1

Statistical analysis of male and female out of total number of subjects

Total Subjects

Male

female

Male 22

Female 08

Total 30


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Graph 2

Comparison of male and female according to their age groups

Table 2

Comparison of male and female according to their age groups

Age Group Male Female

50-60

3 260-70

10 6

70-80

9 0Total

22 8

0

1

23

4

5

6

7

8

9

10

50-60 60-70 70-80

3

109

2

6

0

Male

Female


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Table 3

Statistical analysis of pre training and post training step length

Step length Mean SD Paired - t test

Pre 34.37 7.587

p = 0.002

t = -3.415

Post 36.49 7.605

95% confidence interval for difference: -2.814 to -0.7059

t = -3.415 with 29 degrees of freedom; P = 0.002


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Graph 3

Comparison between pre training and post training step length

33.5

34

34.5

35

35.5

36

36.5

pre treatment post treatment

34.73

36.49

Step Length

pre treatment

post treatment


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TABLE 4

Statistical analysis of pre training and post training stride length

Stride length Mean SD Paired - t test

Pre65.62

8.879

p = 0.005

t = -3.053

Post

68.45

9.09

95% confidence interval for difference: -4.72 to -.9329

t = -3.053 with 29 degrees of freedom; P = 0.005


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Graph 4

Comparison between pre training and post training stride length

64

64.5

65

65.5

66

66.5

67

67.5

68

68.5


65.62

68.45

Stride length

pre treatment

post treatment


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TABLE 5

Statistical analysis of pre training and post training freezing

episodes

Freezing

EpisodesMean SD Paired - t test

Pre

2.167

1.262

p = 0.000

t = 6.158

Post

1.6

1.221

95% confidence interval for difference: 0.3785 to0.7549

t = 6.158 with 29 degrees of freedom; P = 0.000


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Graph 5

Comparison between pre training and post training freezing

episodes

0

0.5

1

1.5

2

2.5


2.167

1.6

Freezing Episodes

pre treatment

post treatment


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TABLE 6

Statistical analysis of pre training and post training time taken toresolve freezing

Resolving time Mean SD Paired - t test

Pre 2.49 1.409

p = 0.002

t = 3.448

Post 1.935 1.411

95% confidence interval for difference: 0.2259 to0.8847

t = 3.448 with 29 degrees of freedom; P = 0.002


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Graph 6

Comparison between pre training and post training time taken toresolve freezing

0

0.5

1

1.5

2

2.5


2.49

1.935

Time taken to resolve

pre treatment

post treatment


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RESULT

The total numbers of subjects selected for the study were 30. Only one

group included. All the subjects were evaluated at the start of the treatment and

again re-evaluated after 6 weeks. Significance was calculated by using paired t-

test.

Table 1 one of graph one shows statistical analysis of total number maleand female out of the number of subjects taken for the sample. There are 22

males and 8 females out of 30 subjects this shows incidences of Parkinsons

more in males as compares to females.

Table 2 and graph two shows incidances of freezing with age according to

gender. All the subjects divided into three groups 50-60; 60-70 and 70-80.

Maximum subjects have freezing episodes within 60-70 age group or more i.e.

25 subjects. These result shows that there is increase chances of freezing with

increasing age.

Table 3 and graph 3 shows significant change in pre-treatment and post-

treatment step length as p


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length 65.62 and post treatment mean stride length is , which indicates that stride

length is increased after giving treatment. There is significant difference in stride

length as p


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LIMITATIONS OF THE STUDY

1. Smaller Sample Size.

2. As freezing time is in seconds and milliseconds its difficult to get proper

freezing time.

3. There is more chances of fall while walking anticlockwise, patients

became apprehensive because of this.

4. Limitation of this work is that performance was only assessed immediately

following training


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DISCUSSION

Parkinsons disease is a progressive neurodegenerative disorder whose

cause remains unknown. The pathological hallmark of Parkinsons disease is the

loss of pigmented, dopaminergic neurons of the substantia nigra pars compacta,

coupled with the presence of intraneuclear inclusion bodies known as lewy

bodies. Diagnosis is clinical and is based on the presence of Slowness of

movement, Poverty of movement, Rigidity, Resting Tremor, and Postural

Instability. Other symptoms, such as shuffling gait, muffled speech,

expressionless stare, and drooling are derived from these cardinal symptoms.Patients with PD may also have cognitive dysfunction, psychiatric symptoms (eg,

endogenus anxious) depression, autonomic dysfunction, musculoskeletal

deformities, sensory symptoms, sleep disturbances, and dermatological

problems.

The experimental study of effect walking along the circle on foot prints on

freezing has been carried out on 30 subjects having Parkinsons and freezing astheir main difficult. Patients were diagnosed according to Hoen and Yahr scale.

Also pre and post treatment readings for their step length, stride length, number

of freezing episodes and time taken to resolve the freezing has been noted. Then

they had given protocol to walk along the circle in clockwise and anticlockwise

direction for 6 weeks and 5 days a week i.e. 30 sessions for 5 mins. The

experimental study has shown significant improvement in reducing freezing in

subjects.

The graph 1 of table 1 shows


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CONCLUSION


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