Seminar On

Gait Rehabilitation In

Parkinson’s Disorder

Moderated By: Mr. K. Vijaya Kumar

Submitted By: Priya Kuberan

CONTENTS

Introduction to Parkinson’s disease

Etiology of PD

PD & basal ganglia pathophysiology

Clinical manifestations in PD

Natural progression in PD

Diagnostic criteria and differential diagnosis

Medical and surgical management

Gait disturbances in PD

Assessment of gait characteristics in PD

Rehabilitation in PD

Physical therapy interventions in gait rehabilitation in PD

References

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PARKINSON’S DISEASE

Parkinson’s disease (PD) is a chronic, progressive disease of the nervous

system characterized by cardinal features of tremors, rigidity, bradykinesia

and postural instability. The etiology of Parkinson’s disease is still largely

unknown and it is also referred to as primary or idiopathic Parkinson’s

disease. It is generally believed that a combination of genetic and

environmental factors play a role in the pathogenesis of Parkinson’s disease.

The primary pathology involves the basal ganglia, especially the substantia

nigra.

Dr. James Parkinson first described Parkinson’s disease in 1817, in his

“Essay in Shaking Palsy”, where he wrote “Involuntary tremulous motion, with

lessened muscular power, in parts not in action and even when supported

with a propensity to bend the trunk forwards and to pass from a walking to a

running pace: the senses and intellect being uninjured”. It was only in the

1860s, as Jean-Martin Charcot tried to differentiate tremors of multiple

sclerosis from other disorders, the condition was more recognized and

thoroughly studied. He virtually identified all four cardinal symptoms of

Parkinson’s disease: rest tremor, bradykinesia, rigidity and balance

impairment. Brissaud drew attention to midbrain lesions as the cause for PD,

however, the pathological hallmark of degeneration of the substantia nigra

was described only in the early 20th century by Tretiakoff.

The reported prevalence of PD varies widely among different studies,

mainly because there is no biomarker to confirm the diagnosis. The

prevalence of PD is high above the age of 70 and is higher in individuals

above 85 years of age. It is rare in people prior to the age of 40. PD is more

common in the American and European population, when compared to their

African or Asian counterparts. No firm evidence for racial difference in

prevalence has been found. In terms of gender prevalence, PD is more

common in men than in women.

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Etiology

No definite etiology has been confirmed for primary PD. Most of the cases

are idiopathic, whereas some have been linked to genetic mutations. The

pathology is characterized by dopaminergic neuronal degeneration in the

substantia nigra. Lewy bodies have been found in autopsied brain matter. It is

generally believed that environmental factors, possibly infectious agents,

toxins, drugs or endocrine disorders, could potentially affect and induce the

manifestation of the underlying defects in genetic expression in these

patients. Many cellular mechanisms have been proposed, including oxidative

stress, premature apoptosis, loss of neurotrophic factors, glutamate toxicity,

inflammatory process, mitochondrial dysfunction, neuromelanin degeneration

and so on. Currently, more and more gene mutation foci have been found to

be related to familial PD. Patients with autosomal dominant and autosomal

recessive gene mutations usually present with parkinsonian symptoms at a

younger age and have strong family histories.

Environmental toxins that may be responsible for inducing PD have been

widely investigated and researchers have found an association with rural

living and agricultural work. There is evidence that exposure to pesticides and

herbicides may increase risks. There appears to be an increased risk of PD

association with dietary iron, manganese and heavy metal intake. Folic acid

deficiency is also known to be related to PD.

Parkinson’s Disease and Basal Ganglia Pathophysiology

Neuropathological examination of brain from patients with PD reveals a

loss of pigmented neurons from the pars compacta of the substantia nigra.

These neurons contain neuromelanin and produce the transmitted dopamine.

Loss of 50% to 60% of these cells from the substantia nigra results in critical

dopamine deficiency in the striatum. Involvement is usually bilateral, but

typically uneven in severity, which explains the asymmetric nature of PD

symptoms. Other subcortical nuclei, including locus ceruleus and dorsal vagal

nucleus may also be affected. Dopaminergic cell losses in the pigmented

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brainstem nuclei, the intermediolateral column of the spinal cord, and the

symptheic ganglia are reported, suggesting associated autonomic dysfunction

in PD paients. Lesions in the nucleus basalis and the ventral tegmental area

accounts for the cognitive deficits

Microscopically, concentric hyaline intracytoplasmic inclusions, termed

Lewy bodies, can be found in several subcortical nuclei of the surrounding

basal ganglia. Lewy bodies contain accumulations of α-synuclein ubiquitin and

protein. Involvement of the cortical area may explain the hallucinations,

psychotic symptoms, and cognitive decline in PD.

Voluntary movement is initiated from cerebral cortex and regulated by

complex feedback loops that involve the cortex, thalamus, basal ganglia and

the cerebellum. The basal ganglia consists of the caudate nucleus, putamen,

globus pallidus (interna and externa), subthalamic nucleus and substantia

nigra. The cerebral cortex is the command centre of the brain and it sends

signals to the striatum by two pathways: direct and indirect. The direct

pathway exits from the putamen and reaches the globus pallidus interna

(GPi). The indirect pathway exits from the putamen and reaches the globus

pallidus interna after passing through the globus pallidus externa (GPe) and

subthalamic nucleus.

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The direct pathway is inhibitory in nature and hence its increased activity

leads to a rise in the inhibition in the GPi, which thereby leads to a

disinhibition of their projections to the thalamus. Increased activity in the

indirect pathway activity causes an increase in the excitation of the

subthalamic nucleus, which leads to augmented inhibiton from the GPi/ SNr to

the thalamus. The dopaminergic system in the basal nuclei has a powerful

modulatory control over the motor system. These nuclei in putamen, GPi and

GPe use GABA as the primary neurotransmitter, which functions as an

inhibitory function to the postsynaptic neurons. Dopamine in the substantia

nigra regulates the putamen by using different dopamine receptors to

enhance the GABA effect on the direct pathway and attenuate the GABA

effect on the indirect pathway. Thus, a decreased dopamine level will cause

disinhibition of subthalamic nucleus and GPi and subsequently inhibit output

from the thalamus to the cerebral cortex, leading to various motor

manifestations of parkinsonism, including resting tremor, bradykinesia and

rigidity. This basal ganglia circuit theory also becomes the pathophysiological

basis for the surgical treatment of PD.

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Clinical Manifestations

Parkinson’s disease is a complex neurodegenerative disorder. Although

the main symptoms are caused by the disrupted control of body movement,

there are many concomitant non-motor symptoms, including cognitive decline

and psychiatric manifestations.

The four main motor symptoms of PD are resting tremor, bradykinesia, rigidity

and postural instability. Generally the presence of resting tremor in addition to

one of the other symptoms, or the presence of the other three symptoms in

the absence of resting tremor, will indicate the clinical diagnosis of PD. Other

supportive diagnostic features are good response to levodopa treatment and

the presence of dyskinesia after long term usage of levodopa.

Motor Symptoms

Resting Tremor

Tremor is usually the first symptom noticed by patients or their family

members. It occurs in the resting position and disappears or diminishes on

hand motions, especially in the early stages of the disease. The frequency is

typically slow, about 4 to 6 Hz. Hands are the most common anatomical sites

with tremor. In addition, legs, chin, mouth and tongue may also be affected. It

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often starts on one side of the body and gradually involves the other side as

the disease progresses. However the side with the initial symptoms is usually

more severely affected and the tremor remains asymmetric throughout the

course of the disease. Flexion of the fingers and rotation of the wrist joint

during tremor are characteristic. Amplitude will vary and become more

pronounced when the patient is under stress. In some patients, after a short

disappearance of their tremor when their hands are held in front of the body, a

postural tremor with the same frequency as their resting tremor may appear.

This is called re-emerging tremor and is characteristic of PD.

Bradykinesia

Bradykinesia refers to slowness of movement and is the most characteristic

clinical feature of PD, although it may also be seen in other disorders,

including depression. Bradykinesia is a hallmark of basal ganglia disorders,

and it encompasses difficulties with planning, initiating and executing

movement and with performing sequential and simultaneous tasks. The initial

manifestation is often slowness in performing activities of daily living and slow

movement and reaction times. This may include difficulties with tasks

requiring fine motor control (eg, buttoning, using utensils). Other

manifestations of bradykinesia include loss of spontaneous movements and

gesturing, drooling because of impaired swallowing, dysarthria, loss of facial

expression (hypomimia) and decreased blinking, and reduced arm swing

while walking. Given that bradykinesia is one of the most easily recognisable

symptoms of PD, it may become apparent before any formal neurological

examination.

Assessment of bradykinesia usually includes having patients perform

rapid, repetitive, alternating movements of the hand (finger taps, hand grips,

hand pronation–supination) and heel taps and observing not only slowness

but also decrementing amplitude. In common with other parkinsonian

symptoms, bradykinesia is dependent on the emotional state of the patient.

Although the pathophysiology of bradykinesia has not been well delineated, it

is the cardinal PD feature that appears to correlate best with degree of

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dopamine deficiency. This is supported by the observation of decreased

neuronal density in the substantia nigra in elderly patients with parkinsonism

regardless of PD diagnosis. It is hypothesised that bradykinesia is the result of

a disruption in normal motor cortex activity mediated by reduced

dopaminergic function.

Rigidity

Rigidity is characterised by increased resistance, usually accompanied by

the ‘‘cogwheel’’ phenomenon, particularly when associated with an underlying

tremor, present throughout the range of passive movement of a limb (flexion,

extension or rotation about a joint). Cogwheel rigidity is a ratchet-like quality

felt when patients’ joints are passively moved. It may occur proximally (eg,

neck, shoulders, hips) and distally (eg, wrists, ankles). Reinforcing

manoeuvres (eg, voluntary movements of the contralateral limb), known as

the Froment’s manoeuvre, usually increase rigidity and are particularly useful

in detecting mild cases of rigidity. Simultaneous co-contraction of agonist and

antagonist muscles may occur, and this is reflected in an immediate

resistance to a reversal of the direction of movement around a joint. Rigidity

may be associated with pain, and painful shoulder is one of the most frequent

initial manifestations of PD although it is commonly misdiagnosed as arthritis,

bursitis or rotator cuff injury. Rigidity also causes stooped posture and forward

shift of the center of gravity (propulsion), resulting in postural instability.

Patients also manifest flexed limbs and decreased arm swing when walking.

Postural Instability

Postural instability is likely to be the combined effect of rigidity and

bradykinesia and generally occurs in patients with more advanced PD. It is

mainly due to the loss of postural reflexes, which causes difficulties in

positional adjustments. The patient’s trunk is flexed to the stooped posture,

and he or she presents with shuffling gait. The patient with PD tends to walk

more quickly due to involuntary propulsion and he or she might take smaller

or faster steps and fall forward as a result. The symptoms resulting from

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postural instability are unfortunately relatively resistant to pharmacological

treatment.

Non-Motor Symptoms

Motor difficulties are not the only problems for PD patients. a variety of

non-motor symptoms that lessen the patient’s quality of life include psychiatric

symptoms (depression, anxiety), autonomic dysfunctions, sleep disturbances,

sensory disturbances (especially pain), and dementia.

Cognitive impairment

Dementia in PD may not be evident until the later stages. Although the

cognitive decline reported in early stage PD is subtle and does not often

interfere with daily functioning, PD patients have been shown to demonstrate

cognitive slowing and executive functioning problems at early stages. PD

related cognitive deficits have also been observed in language, visuospatial

functioning, long-term memory and executive functioning.

Psychosis

Hallucinations may occur during later stages of PD. Psychosis and visual

hallucinations are commonly related to dose-dependent adverse effects of

anti-Parkinsonian drugs in combination with disease progression and medical

illnesses. Auditory hallucinations are rare.

Depression

Depression is a very common feature in patients with PD with prevalence

being 16%-70%. Norepinephrine and serotonin play important roles in

depression by linking with dopamine deficiency. The depression is

characterized by decreased energy and motivation, loss of interest, feeling of

sadness, helplessness and hopelessness, change in sleep, weight and

appetite, irritability. The patient may fluctuate between a normal affect and a

depressive state, with more frequent episodes of depression during the “off”

stage of medication and improvement when motor symptoms are better

treated. They also experience periodic anxiety and panic attacks which

substantially contribute to morbidity.

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Sleep Disturbance

Sleep disturbance is a common problem in PD patients and is usually

associated with depression and hallucinations. Patients may suffer from

restless leg syndrome, which can cause insomnia. REM behaviour sleep

disorder is very likely to occur and is characterized by loss of atonia during

REM sleep, resulting in excessive motor activity during dreams. This is also

an indicator of presymptomatic PD.

Autonomic Dysfunctions

These include orthostatic hypotension, excessive drooling, constipation,

regurgitation, decreased gastrointestinal functionality, urinary frequency or

incontinence, sexual dysfunction and excessive sweating or intolerance of

heat and cold.

Natural Progression of PD

The progression of PD varies among patients. It affects the upper and

lower limbs asymmetrically and eventually most patients will be affected on

both sides. The initial symptoms are usually mild. The signs maybe usually

subtle and patients may only experience slowness, stiffness and difficulty with

handwriting. Eventually, patients will experience asymmetry of parkinsonian

signs, obvious resting tremors and a clinically significant response to

levodopa. The speed of progression varies but maybe related to different

subtypes. Clinical subgroups are often classified into tremor-dominant versus

postural instability gait disorder variants. Another group is young-onset and

late onset PD. When PD begins in an elderly patient, decline is more rapid

than in middle-aged onset patients and bradykinesia, rigidity and balance

problems predominate over tremor. The tremor-predominant patients

generally have a slower decline in motor function than the akinetic/rigid ones.

Young-onset patients have more preserved cognitive function and fewer falls

than those with late disease onset.

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The responses to medical treatment vary individually. However, most of

the PD patients will benefit from dopaminergic medications, especially in the

beginning stages of the disease. During the moderate stages of PD, although

patients are still having good responses to dopaminergic medications, they

may gradually need more doses or a combination of medications to maintain

their motor functioning.

The major problem that most patients experience after years of treatment

for PD is symptom fluctuations. The most common form of motor fluctuation is

a predictable decline in motor performance occurring near the end of each

medication dose. As time goes on, many patients experience involuntary

choreiform movements, called “on-time dyskinesia” as a peak dose

complication after medications are taken. This on-off fluctuation not only

severely affects the patient’s quality of life but also becomes a challenge

during the management.

Diagnostic Criteria and Differential Diagnosis

There is no single laboratory or imaging test to confirm the diagnosis of

PD. Pathological diagnosis depends on finding Lewy bodies in an autopsied

brain. A commonly accepted diagnostic criteria is the finding of at least 2 out

of 3 cardinal symptoms of resting tremor, bradykinesia or rigidity in the

absence of other apparent causes of parkinsonism.

Response to levodopa can be used as a diagnostic indicator of likely

primary PD. Conventional brain imaging such as CT or MRI scans is not

useful for the diagnosis of PD. Positron emission tomography studies using

18F-fluorodopa demonstrates reduced uptake in the striatum, particularly

marked in the putamen in PD patients. using single photon emission

computerized tomography (SPECT) with dopamine transporter ligands, the

level of dopamine in the basal ganglia can be quantitatively measured and a

deficiency will indicate PD.

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The differential diagnosis of PD covers a broad range of disease

categories. Any condition presenting with parkinsonian symptoms should be

considered for primary PD, secondary parkinsonism or parkinsonism plus

syndromes. Parkinsonism plus syndrome, is mostly idiopathic. This includes

progressive supranuclear palsy, multiple system atrophy, corticobasal

degeneration and dementia with Lewy bodies.

Medical Management

Medications are used to compensate dopamine deficiency resulting from

degeneration of the substantia nigra. These include the dopamine precursor

levodopa, dopamine agonists and dopamine stimulating agent amantadine.

Anticholinergic agents such as trihexyphenidyl reduce tremor by restoring the

imbalance between acetylcholine and dopamine levels in the brain. MAOB

inhibitors may have symptomatic and neuroprotective effects. Catechol-O-

methyltransferase inhibitor acts to prolong and stabilize dopamine levels by

reducing its metabolism.

Levodopa is the most efficacious medication for treatment of PD. It is the

precursor of dopamine that will be converted by dopa-decarboxylase to

dopamine once it is transported through the blood brain barrier. Levodopa is

administered orally in three or more divided doses throughout the waking

hours.

Dopamine agonists have high affinities to dopamine receptors and mimic

its action by binding onto them. They are used as a primary drug treatment for

PD or as an adjunct to levodopa. Their clinical efficacy is well established.

Dopamine agonists are many times used as an initial treatment in newly

diagnosed patients with PD or used as a combination therapy with levodopa.

Apomorphine is a rapidly acting dopamine agonist.

COMT is widely distributed in the glial cells in the human brain. Most of the

levodopa absorbed into the body is converted by COMT to the inactive

metabolite 3-O-methyldopa before crossing the blood brain barrier into the

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brain. The accumulated 3-O-methyldopa then competes with levodopa

absorption in the gut and the blood vessel wall, resulting in levodopa level

fluctuations. COMT inhibitors like entacapone and tolcapone, inhibits this

enzyme and are hence used as adjunctive therapy with levodopa to curb the

end-dose wearing off effect of the drug.

MAO inhibitors like selegiline and rasagiline are the only available

medications in this category. They are used to inhibit the enzymatic

degradation of dopamine by MAO-B in order to prolog its duration of action.

Anticholinergics like trihexyphenidyl is known to be effective in controlling

resting tremor which is caused by dopamine-acetylcholine imbalance.

Amantadine is used to stimulate dopamine release and inhibit glutamate

neurotransmission in order to improve tremor, rigidity and bradykinesia in

early stage PD patients.

Surgical Treatments

Thalamotomy : removal of intermediate nucleus of the thalamus, preferably,

unilateral to reduce Parkinsonian tremor

Pallidotomy: removal of globus pallidus

Subthalamotomy: removal of subthalamus

Deep brain stimulation: involves a surgically implanted, battery-operated

medical device called a neuro-stimulator that delivers electrical stimulation to

strategic areas of the brain to block abnormal signals inn the circuitry of the

basal ganglia and reduce PD symptoms.

Thalamic DBS, Subthalamic DBS, Pallidal DBS

Brain transplantation (autologous adrenal medulla transplantation to the

caudate nucleus) is also an option considered by a few surgeons.

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Gait Disturbances in Parkinsonism

The gait disturbances in PD may be divided into two types:

1. Episodic.

2. Continuous

The episodic gait disturbances occur occasionally and intermittently,

surfacing in an apparently random, inexplicable manner. The episodic gait

disturbances include festination, start hesitation, and freezing of gait. The

latter is a debilitating phenomenon that is most commonly experienced by

patients with advanced PD. Conversely, the continuous changes refer to

alterations in the walking pattern that appear, at least at first glance, to be

more or less consistent from one step to the next, i.e., they persist and are

apparent all the time. While both types of gait disturbances are a result of

basal ganglia dysfunction and certain episodic symptoms are associated with

other continuous symptoms e.g., patients with freezing of gait have increased

gait variability, the specific mechanisms responsible for the episodic and

continuous gait disturbances are likely somewhat independent. Here we focus

on the continuous gait disturbances, in part, because they are more prone to

an analysis that examines the ongoing dynamics.

Classic studies of Parkinsonian gait have focused on the continuous gait

disturbances, especially those that can be readily seen using visual

observation. These include slowed ambulation in part a manifestation of

bradykinesia with decreased or absent arm swing, longer double limb support

i.e., more time with both feet spent on the ground, and impaired postural

control. One of the keys to these gait problems is the inability of patients with

PD to generate sufficient stride length, a problem that has been related to

impaired scaling of amplitude. In fact, the reduced and shortened stride length

may explain many of the continuous gait disturbances in PD including the

reduced gait speed and the increased time with the feet on the ground.

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Parkinsonian gait is primarily characterized by hypokinesia, which refers to

slowness of gait. These patients demonstrate short stride length, decreased

cadence, decreased arm swing and poor ground clearance. The term

shuffling gait is often used to describe how the patients with PD walk. The fear

of falling also contributes to the hypokinetic characteristics of PD gait.

Akinesia is manifested in the inability of PD patients to initiate gait or in

“freezing” during gait. The PD gait also demonstrates decrease in force

generation, dysrhythmicity, left/right dyssynchrony, abnormal preparation and

execution of motor function. In addition the ability to initiate and maintain

locomotion is heavily dependent on postural reflexes, which are frequently

disturbed in PD. The contribution of each disturbance to the final parkinsonian

gait abnormality differs from one patient to another and in the same individual

at different times of the day or stages of the disease.

Parkinsonian gait demonstrates that basal ganglia dysfunction affects not

only the automatic maintenance of the scale of movement (motor set) but also

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the running of each component of the motor plan in a timely manner (cue

production)

Gait Initiation

Initiation of gait can be subdivided into a movement preparation period and

a movement execution phase. Movement preparation represents the motor

planning phase, in which an overall strategy is taken as to where, when and

how to initiate gait. In PD patients, the preparation time was found to be

significantly prolonged, with a tendency to become longer as the disease

progressed. Execution time was prolonged as well, but to a lesser extent.

During gait initiation, posture is adjusted first by shifting the center of

gravity laterally and rotating the body before weight is taken on the stance foot

to allow the leading leg to swing forward while the COG is shifted anteriorly to

create the forward momentum. This shift in the COG anteriorly is

accomplished by bending the trunk and ankle. The onset of the anterior shift

of the trunk was found to be slow in patients with advanced PD. In addition

there is reduced lateral shift of the body mass over the stance limb,

decreased propulsive force and prolonged anticipatory postural adjustment.

All of these motor deficits reported in PD patients are most pronounced in

self-initiated gait. Disturbances in gait initiation is directly related to

dysfunction of the basal ganglia to control internally cued movement

sequences, delaying onset but not slowing down the execution or altering the

pattern of movement components

Freezing

Freezing, also referred to as motor blocks, is a form of akinesia (loss of

movement) and is one of the most disabling symptoms of PD. Although

freezing is a characteristic feature of PD, it does not occur universally. It

occurs more frequently in men than in women and less frequently in patients

whose main symptom is tremor. Freezing most commonly affects the legs

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during walking, but the arms and eyelids can also be involved. It typically

manifests as a sudden and transient (usually,10 s)inability to move. This may

include hesitation when beginning to walk (start hesitation) or a sudden

inability to move the feet during specific situations (eg, turning or walking

through a narrow passage, crossing busy streets, approaching a destination).

Freezing is associated with substantial social and clinical consequences for

patients. In particular, it is a common cause of falls.

Five subtypes of freezing have been described: start hesitation, turn

hesitation, hesitation in tight quarters, destination hesitation and open space

hesitation. Episodes are more severe in the OFF state and are mitigated by

levodopa therapy. In addition, patients often develop tricks to overcome

freezing attacks. This includes marching to command, stepping over objects

(eg. a walking stick, cracks in the floor), walking to music or a beat, and

shifting body weight. Risk factors for the development of freezing include the

presence of rigidity, bradykinesia, postural instability and longer disease

duration. In contrast, tremor at disease onset is associated with a decreased

risk of freezing. Freezing, particularly when it occurs during the ON period,

does not usually respond to dopaminergic therapy, but patients treated with

selegiline have been found to be at lower risk. Botulinum toxin injections,

although effective for a variety of parkinsonian symptoms such as tremors,

dystonia and sialorrhoea, have not been found consistently effective in the

treatment of freezing.

Freezing episodes have been divided into

a) no movement-akinesia (the patient is not making any observed effort to

overcome the block)

b) trembling in place (rapid synchronized movement of both legs

observed as the patient attempts to overcome the block but no

movement forward is seen)

c) shuffling forward (the patient makes an effort to overcome the block

and is partially successful but the steps are very small and rapid and

no real step is taken)

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Start hesitation

Start hesitation is the classic parkinsonian disturbance experienced at gait

initiation. It has been described as the most common type of freezing of gait

and is now considered to be part of the episodic gait disturbances. The

patients describe start hesitation as a “feeling that their feet are stuck or glued

to the ground.” It is frequently seen at initiation of gait but also occurs while

changing from one mode of movement to another.

Although an episode of start hesitation generally lasts a few seconds, it

can sometimes last long enough to make gait impossible. During the “on”

state, start hesitation usually lasts a few seconds and is easily overcome.

During the “off” state, start hesitation lasts much longer and is more difficult to

overcome. During these episodes, patients are actively trying to overcome the

block by making small and ineffective movements with their legs. In the worst

case, this situation can lead to falls.

The mechanism responsible for start hesitation is not clear, but it has been

associated with a complete lack of initiation of postural adjustments. After

recording the leg muscle activation of PD patients during freezing episodes, it

has been found that there is co-activation of the agonist and the antagonist

muscles without the temporal activation pattern seen in normal gait initiation.

Such a disturbance of muscle activity can explain the inability to initiate a

step.

Turning hesitation

Turning around while walking is most problematic for people who

experience episodes of freezing or motor instability. Usually when elderly

people perform a 360-degree turn during walking, they take fewer than 6

steps to complete the action. In contrast, those with PD and motor instability

take up to 20 steps to turn, with each step becoming smaller and smaller until

they eventually stop. In addition, people with PD show little movement of the

trunk, head, and arms when turning, whereas people without movement

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disorders turn by moving the head, shoulders, trunk, and legs in a fluid

sequence.

Festinating Gait

Festinating gait is another typical disturbance of locomotion in

parkinsonian patients. its frequency is undetermined but it is known to be

more common in older patients and those with advanced PD. It consists of

rapid small steps taken in an attempt to keep the COG above the feet while

the trunk lens forward involuntarily and shifts the COG forward. To

compensate and in an attempt to prevent falling, the patient increases

stepping velocity and further shortens the stride. Rather than representing

compensatory steps for an increasing loss of step amplitude, festination may

also be a primary deficit related to freezing. The increased step frequency

combined with minimal step amplitude may reflect an involuntary rhythmic

loss of control of gait. Freezing is often preceded by festinating steps, thereby

establishing that freezing and festination are related phenomena.

Arm Swing

One of the clinical features associated with PD is decreased arm swing. It

is frequently an early sign of the disease. The reduction in upper limb

movements in PD patients is associated with a significantly delayed onset of

arm swing, reduced length of the arm cycle, and reduced velocity of arm

swing in the gait cycle. Decreased arm swing while walking is a part of

hypokinesia and is also influenced by rigidity.

Gait Termination

Gait termination occurs as the result of decelerating the forward motion of

the center of mass. In the patients with PD, a decreased ability to internally

control changes in the center of mass during self-directed activities such as

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getting up from a chair, turning, or stopping is commonly associated with falls.

Understanding how one stops, therefore, has implications for people who may

be at risk of injuring themselves as a result of their inability to stop effectively.

When healthy adults are rapidly terminating gait, the muscle activity

generated in response to the cue to stop is produced by a flexible set of motor

commands in the stance limb, and by a single motor program in the swing

limb. Difficulty in activating this program in PD patients will affect his ability to

stop. Additionally freezing of gait will lead to involuntary termination of gait,

which is a transient phenomenon common to patients with PD.

Three phases of planned gait termination have been identified: preparatory

brake, fast brake and final brake. The goal of preparatory braking is described

as the reduction of forward velocity and adjustment of posture for ensuing

phases. During fast braking, a rapid reduction in kinetic energy occurs. In the

final brake phase, the remainder of forward velocity is educed as the center of

pressure moves quickly ahead of he center of mass due to increased activity

of the plantarflexors and finally the center of mass is brought within the base

of support.

Patients with PD tend to slow their gait velocity earlier than the healthy

adults would. These patients slow down their velocity several steps earlier

than their healthier peers and enter the final step at only 84% of forward

velocity. An unplanned stop may be defined as the termination of gait that

occurs without prior planning. Those with PD modulate the braking impulse

generated under the stance limb differently. Subjects with PD show patterns

of muscle activation that differ when comparing planned and unplanned

stopping when, in contrast, it appears that healthy adults use similar patterns

in both.

The PD patients also demonstrated differing patterns of muscle activation

between tasks. During planned stopping, these subjects increased distal leg

muscle activity of the stance limb, resulting in the co-contraction at the ankle

and when stopping was unplanned, subjects decreased tibialis anterior

activation and increased soleus activation of stance limb. During unplanned

stopping, they also increasingly activate soleus of the swing limb to a greater

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extent. Difficulty in stopping has been related more to functional measures like

gait speed than disease severity. PD patients tend to take more steps when

stopping suddenly. Also there has been observed alternating bursts of tibialis

anterior and soles activity in slower walkers

Kinematics

PD gait is characterized by reduced joint angular excursions. This is mainly

true at the ankle joint in the initial stages of the disease but not very apparent

at the knee or the hip joints. Most important, plantarflexion (but not

dorsiflexion) is decreased in PD and consists of a reduction in ROM during

push-off and a reduction in plantarflexion at toe-off. As the disease

progresses, the proximal joints also lose their normal range and contribute in

the gait disturbances

Kinetics

Abnormality in the pattern of the kinetics is more pronounced than in the

kinematics. This discrepancy may be related to the fact that similar kinematic

patterns can be produced by different underlying kinetics. At the ankle joint,

the moment at loading response (dorsiflexion moment) is reduced in the PD.

This could occur if the ground reaction force vector remained close to the

ankle joint. Hypothetically, this is possible if, at initial contact, the subjects with

PD had limited hip flexion, inadequate knee extension, or absent heel strike.

Although joint angular values at initial contact are highly variable, the PD

patients have increased range of knee flexion (with consequent inadequate

extension) and lesser hip flexion. As a result, a smaller heel rocker would

ensue with a consequent flat-footed gait pattern.

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Variability in Parkinsonian Gait

Gait disturbances in PD also include features that are not always easily

quantifiable in routine clinical observation but become apparent when gait is

evaluated quantitatively with gait analysis systems. Such changes include

increased left-right gait asymmetry and diminished left-right bilateral

coordination. A loss of consistency in the ability to produce a steady gait

rhythm, resulting in higher stride-to-stride variability, is also a characteristic

feature of gait in PD. Increased gait variability can be seen throughout the

disease, even in patients who were only recently diagnosed with PD, who

have very mild disease and have not yet started to take anti-Parkinsonian

medications.

The magnitude of the variability also tends to increase with disease

severity. This gait feature is of interest for a number of reasons. First, unlike

features such as gait speed, swing time, or double support time, which are

based on average values or the first moment of a gait time series, variability

measures reflect the second moment, and are, to a large degree, independent

of stride length, both theoretically and experimentally. Gait variability, also

referred to as unsteadiness or inconsistency and arrhythmicity of stepping,

has also been found to be one aspect of walking closely associated with risk

of falls in the elderly, even more so than measures based on the average

value of a given gait parameter. Impairment in the ability to maintain a steady

gait, with minimal stride-to-stride variations, is not only closely related to

postural instability and fall risk; it is largely independent of gait speed and

healthy-aging effects.

History of Falls In PD

Any of the above disturbances in gait can lead to frequent falling in patients

with PD. It has been established that falls were more frequent in patients with

PD than in patients with other neurological disorders. Disturbed gait was

associated with 55% of falls in individuals with PD. The fallers report an

average of 3-5 falls in a year. The fallers were also more impaired and had

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poorer measures of mobility and balance than the non-fallers. Patients with

PD who fall tend to take more steps to complete a task of mobility, had

reduced functional reach and greater postural sway when completing dual

tasks. Also the stride to stride time variability was greater indicating more

impairment both on and off medications in individuals who fall. Thus frequent

falls, mostly due to intrinsic factors, result in restriction of activity.

Factors Affecting Gait In PD

Bradykinesia

Rigidity

Cognition: Cognitive deficits like impaired visuospatial skills and poor

executive functions severely affect the planning and execution involved

during gait initiation and execution in PD patients.

Psychiatric status

Stage of the disease: The gait characteristics are known to have

worsened in accordance to the severity of the disease.

Drugs: The gait of the PD patients is known to be markedly improved

during the “ON” phase of the drug effects.

Assessment of Gait Characteristics in PD

Gait should be assessed in every PD patient as part of the basic

evaluation at the initial and all follow-up evaluations. Scales like the Unified

Parkinson’s Disease Rating Scale comprehensively measures individual

motor and non-motor symptoms in PD. Thus the motor skill component of the

UPDRS can be used to measure gait and some of the factors influencing it.

This scale also measures the non-motor symptoms of PD and thereby can

help us develop a complete picture of all aspects of gait.

Besides the UPDRS, there are other components that have to be

assessed when we assess the gait of a PD patient.

i) Gait speed

ii) Cadence

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iii) Stride length

iv) Time to turn 360 degrees

v) 5-step test

vi) Functional reach test

vii) Berg Balance Scale

Two timed tests of gait can be used to assess the performance, the 10-m

walk test and the “timed up and go” test. Both tests have established validity

and reliability in both the home and clinical setting for patients with PD. In both

the tests it is important to be explicit about the speed with which the task

should be accomplished. The patient should be asked to walk at whatever

speed feels more comfortable. While the patient is performing the task, the

examiner should assess the patient’s ability to initiate gait, keep an upright

position, walk towards a destination, perform a turn in place and return to the

chair correctly. Other features to be observed are body posture, speed and

fluency of stepping, stride length and distance between the feet.

The Tinetti scale is also widely used in order to assess gait and mobility in

PD patients. If the patient is complaining about freezing, then the examiner

should try and provoke freezing episodes. The clinical assessment of gait is

ultimately based on the examiner’s observational impression. For more

detailed and precise evaluation of gait, the assessment takes place in a 3-

dimensional computerized gait laboratory, where cadence, stride length,

velocity and double limb support are measured while obtaining information on

muscle activation, joint movement and analysis of limb movement in space.

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Rehabilitation In Parkinson’s Disease

Parkinson’s disease is chronic and degenerative, therefore interventions

that are put in place at one stage may be insufficient or inappropriate at a later

stage. Thus the process of rehabilitation in Parkinson’s disease is a cyclical

one.

Therapies are harder to define than drug or surgical interventions. The

methods used by therapists are based upon principles but are tailored to the

needs of the individual patient. All therapies have a greater or lesser element

of education and, in order to gain (maximum) effect, patients are expected to

be active participants in their therapeutic programmes. Because of this

individual approach it is hard to define precisely what the intervention consists

of when looking at a population of patients. However, if the principles and the

framework in which they are applied are defined, the disease-specific

techniques are described and the level of evidence to support each practice is

stated, then a set of evidence-based practice guidelines can be produced.

These guidelines can inform therapists in their day-to-day practice and can

also be tested within the context of a trial. Such guidelines have been created

for physiotherapy and are in development for occupational therapy. Speech

and language therapy has general guidelines for the treatment of dysarthria

but they are not specific to Parkinson’s disease.

Physical therapy: the physical therapist evaluates the PD patient’s gait,

balance, range of motion, coordination and transfers. The goal of therapy has

been largely to help people maintain what motor capability they have for as

long as possible and to help them adjust as their functional levels inevitably

decline. It is now recognized that the brain has the ability to reorganize after

disease and it can be facilitated through activity-dependent processes,

including environmental enrichment, forced-use, complex skills training and

exercise.

Occupational therapy: The occupational therapist evaluates the patient’s

occupational performance, or ability to engage in self-care, work and leisure.

The OT looks at both the physical and psychosocial components of activity

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while assessing the patient’s ability to perform ADL tasks. They will instruct

the patients about energy conservation techniques and motion economy

techniques to maximize function.

Speech and Swallow therapy: PD frequently affects breathing, voice

production, the richness of the voice and clarity of speech. A speech and

language pathologist evaluates and treats the patients with such problems.

For swallowing and aspiration prevention is the most crucial aspect.

Dysphagia therapy is also initiated.

Physical Therapy Interventions in Gait Rehabilitation

Physical Therapy for Patients With Newly Diagnosed Parkinson Disease

In the early months after diagnosis, physical therapists have considerable

scope to teach people with PD strategies to optimize locomotor performance

and physical activity prior to the commencement of levodopa medication.

Uniquely, in the “de novo” stage, there is an opportunity to assess the

person’s baseline levels of impairments, activity limitations, and participation

restrictions before medications have commenced. The natural variability in the

person’s capabilities, therefore, can be mapped without the confounding

effects of pharmacological therapies. Baseline data can be retained for future

use in evaluating disease progression. Core strategies can be learned for

moving quickly and easily with large-amplitude movements, and these

strategies can be retained for when they are needed later in the disease

process.

The motor learning literature shows that skills are learned most effectively

when they are practiced repeatedly in relation to meaningful goals,

incorporating variations in the manner in which they are performed and

varying the environment and task. For example, if the goal is to train a person

with gait hypokinesia to walk with long steps, this could be practiced

repeatedly over short (eg, 10 m) and longer (eg, 40 m) distances on different

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walking surfaces (concrete, floor boards, carpet, grass, uneven ground,

slopes) at slow, medium, and fast speeds. The person with mild PD also could

be encouraged to walk with long strides on wide and narrow pathways,

incorporating turns of different magnitude (eg, 60°, 120°, 180°) rather than

simply performing straight-line walks.

From the outset, it is recommended that information be provided about

falls prevention, the future risk factors for falls, and how to modify the

environment and task performance in order to avoid slipping, tripping, and

falling. Activities such as walking, cycling, golf, tai chi, and bowling also can

be practiced. Another priority is to educate people with PD and their

“significant others” about the benefits of regular physical activity and how to

incorporate into their life a daily exercise and mobility routine.

Physical Therapy After Levodopa Is Commenced

On commencement of levodopa or other PD medications, the physical

therapist acquires several new roles. The first new role is to evaluate the

person’s response to the medication by conducting a dose-response trial. This

involves measuring impairments of body function and activity limitations at

close and regular intervals across a 24-hour period when the person is both

“off” and “on” his or her medication.

Gait Training Strategies

Gait training focuses on primary gait impairments, which typically include

slowed speed, shuffling gait pattern, diminished arm swing and trunk

movements and an overall attitude of flexion while walking. Training programs

have to be designed to lengthen stride, broaden base of support, improve

stepping, improve heel-toe gait pattern, increase contralateral trunk

movement and arm swing, increase speed and provide a program for regular

walking.

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Physical therapy aims to teach people with PD how to minimize the disabling

effects of motor and sensory impairments in order to enhance participation in

societal roles and quality of life.

Relaxation exercises

Gentle rocking can be used to produce generalized relaxation of excessive

muscle tension due to rigidity. Slow, rhythmic, rotational movements of the

extremities and the trunk should often precede gait training. The PNF

technique of rhythmic initiation, in which movement progresses from passive

to active-assistive to lightly resisted or active movement has been specifically

designed to help overcome the effects of rigidity in PD. Additional strategies to

promote relaxation include an emphasis on diaphragmatic breathing during

exercise. Patients may also benefit from cognitive imaging or meditation

techniques or conscious recognition and release of muscle tension.

Stress management techniques are an important adjunct to relaxation. A

daily schedule needs to be planned to accommodate the restrictions of the

disease and the functional needs of the patient. Lifestyle modifications and

time management techniques reduce anxiety associated with movement

difficulties and prolonged times required to complete basic functional tasks.

Flexibility Exercises

Both active and passive range of motion exercises are used to improve

flexibility. Ideally ROM exercises emphasize active motions that are

performed two or three times a day. Passive ROM exercises work within the

patient’s available ROM to maintain range. Since these patients have limited

energy to expend and multiple clinical problems, they may benefit from ROM

exercises in physiological patterns of motion.

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PNF patterns can be used combining several motions at once while

emphasizing on rotation, a movement component that is lost early in PD. In

the upper extremities bilateral symmetrical D2 flexion patterns are ideal in

promoting upper trunk extension and in counteracting kyphosis. In the lower

extremities, hip and knee extension should be emphasized ideally in a D1

extension pattern to counteract the typical flexed, adducted position of the

lower extremities. ROM exercises should also emphasize on restoring range

in the neck and trunk and can be performed in combination with rotational

exercises to promote relaxation.

Strength Training

Strength training has been known to improve strength and motor function

in patients with early stages of PD. Greater improvements have been seen

while using a combined program of balance training and high intensity

resistance training. Strengthening exercises should be timed for “on” periods

after drug, when the patient is at his or her best. Strength training, especially

for the muscles of the lower limb and trunk have known to enhance the gait

characteristics in PD patients. Strengthening exercises targeting the knee

flexors and extensors, hip muscles and ankle dorsiflexors would improve the

patient’s gait remarkably.

Isokinetic strength training has shown good benefits in patients with PD.

Isometric training is discouraged in these patients as there is already

excessive co-contraction and coactivation in these patients.

Functional training

The PD patient often finds it difficult to perform activities of daily living due

to the various clinical manifestations. Transitions like sit-to-stand and activities

in standing are all very poor in these patients, especially as the severity of the

disease increases. Thereby functional training should also precede gait

training.

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Balance training in Patients with PD

Improving balance in individuals with PD is a common goal. And a lot of

strategies can be incorporated into the physical therapy intervention program

to improve both static and dynamic balance. Balance training can consist of

basic perturbations, unilateral stance, functional balance exercises,

manipulation of visual and support surface environments, targeted sway

activities. A series of progressively more challenging spinal flexibility

exercises can lead to an improvement in balance.

An improvement in the static as well as dynamic balance can lead to an

increased walking speed, decreased cadence and reduce the number of falls

in PD patients, thereby improving their gait.

Cueing

Cueing can be defined as using external temporal or spatial stimuli to

facilitate movement (gait) initiation and continuation. Recent reviews on

cueing suggest that it can have an immediate and powerful effect on gait

performance in people with Parkinson’s disease, indicating improvements in

walking speed, step length and step frequency. The influence of cueing has

mainly been studied in single-session experiments in laboratory settings.

Results show a short-term correction of gait and gait initiation, and suggest

that carry-over to uncued performance and its generalisation to activities of

daily living (ADL) is limited. Using cues in a therapeutic setting is more

complex, as the ‘‘modality’’ of cue delivery (visual, auditory or somatosensory)

and the cue ‘‘parameter’’ selected for movement correction (frequency or size

of step) have to be adapted to the needs of the patient. Use of external

auditory and visual cues can improve gait by directing attention to the task of

walking. Furthermore, cognitive strategies (internally generated cues such as

thinking about the size of a step) are equally as effective as external visual

spatial cues.

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The complexities of home and community environments and the multitask

nature of functional activities may interfere with one’s ability to focus attention

and may limit the use of attentional strategies in certain situations. In addition,

attentional strategies potentially have a high cost in terms of mental effort and

fatigue as a result of using cognitive resources to generate the attentional

cue. External cues may therefore require less effort and attention, and their

use during more complex activities could facilitate walking. The distinction

between attentional cueing strategies that must be generated internally

through cognitive processes (such as thinking about the movement or size of

a step) and external cues (auditory rhythmic tones) may therefore be

important. A combination of cueing strategies may prove useful to address the

wide variety of situations encountered and different levels of ability.

Visual cueing is a subtype of cueing wherein the patient is made to walk

based on cues he can see. They can be:

a) Lines on the floor

b) Footprints on the floor

c) A flashing rhythmic light at the side of glasses

Auditory cueing can be in the form of audible, loud, rhythmic beeps that the

patient can clearly hear.

Somatosensory cueing is in the form of a miniature vibratory cueing device,

which can be attached to the wrist.

In the cueing conditions, subjects are asked to synchronize each step with

either the auditory tone or the flash of light. The effects of cues on gait are

well documented, with increases observed with auditory rhythmic, visual

spatial, and verbal cues. Rhythmic cues at frequencies (typically 10%) above

a subject’s preferred stepping frequency result in increased walking speed,

mean step length, and step frequency, the results being shown in single task

conditions. The use of an external (rhythmic) cue during the functional task

reduces gait interference because it demands less attention than when

performing the task with no cue, which requires someone to use cognitive

32

processes to efficiently divide attention between tasks, thus enabling the

patients to perform dual tasks effectively.

Cueing, in general, increases the step length in PD patients and also their

walking speeds. Cueing also has known to reduce episodes of freezing in

laboratory settings, but their long term carry over effect in the external

environment is yet to be firmly established.

Mechanism of external cueing

Dual tasks interfere with gait in people with PD. It is suggested that this

results from increased competition for attention because of defective basal

ganglia function, which requires subjects to use increased cognitive resources

to both walk and do a concurrent task. Additionally, it has been reported that

the beneficial effects of visual and attentional cueing strategies disappeared

when additional tasks were performed; thus the cues required constant

monitoring to maintain their effect. PD subjects can take advantage of

advance information explicitly provided by a cue compared with internally

generated strategies. Movement occurs as a feedback response rather than

as an internally generated response that uses an attentional strategy that

requires planning and feed-forward motor control. The external cue allows

executive processes to facilitate selective attentional processes under frontal

cortical control. The need to select the correct response, initiate theresponse,

and maintain initiation throughout the task is removed, which potentially frees

up attentional resources. The relative cost of external and attentional cueing

in terms of effort may, therefore, be very different. This may not be apparent

when the task is simple or performed in relative isolation.

However, when additional activities are performed, the mental effort

required will increase and under these circumstances motor performance may

decrease. It is argued that in these situations, such as real-world conditions,

the distinction between an external cue and an attentional cued strategy may

become more apparent. Rhythmic cues may act as temporal cues, replacing

defective, internally generated cues (discharges) of the basal ganglia. The

frequency of an auditory cue is important but the timing at which the cue is

delivered in the movement sequence is also important. Cues delivered later in

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the movement facilitated performance more than did cues delivered earlier,

thus the timing of the movement cycle is critical. These experiments, however,

were performed in the upper limb. It is yet to be determined whether the

issues of cue timing in relation to the movement are as beneficial in the

walking cycle. This may point to the need to refine the delivery of cues; thus

the frequency and specific instruction about the use of the cue during walking

may maximize its effect.

Verbal Instructions

People with Parkinson’s disease need to constantly pay attention to

aspects of walking that are difficult in order to walk normally and safely. For

instance, paying attention to taking big steps, walking fast, counting in rhythm

while walking, swinging arms while walking and putting heels down while

walking are strategies often used by people with Parkinson’s disease.

‘Attention’ is defined as ‘focusing on certain aspects of current experience

to the exclusion of others. It is the act of heeding or taking notice or

concentrating.’ Attention is a cognitive process, which can be prompted by

verbal instructions (verbal commands given by another person). Verbal

instructions are convenient and, unlike visual and auditory cues, require no

equipment.

The verbal instructions will consist of normal gait characteristics that the

patients with PD will lack. A few examples of basic verbal instructions used

during gait training are:

a) Take big steps

b) Walk fast

c) Swing your arms while walking

d) Count your steps

e) Walk fast with big steps

f) Look forward while walking

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Evidence found suggests that the outcome of verbal instructions may be

instruction-specific. People with Parkinson’s disease were commanded to

take big steps and consequentially this aspect of gait (stride length)

increased. Attention strategies are traditionally recommended for people with

Parkinson’s disease who do not have severe cognitive impairment, as

impaired cognitive function may limit one’s capacity to enlist attention and

subsequently increase falls risk. People with Parkinson’s disease who have

severe motor complications may require more attention to walking, and it is

possible that they would respond differently to the attention strategy.

Treadmill Training

The relative merits of treadmill training in gait rehabilitation for PD patients

has been established in various studies. Gait training on the treadmill with or

without body weight support has been known to produce a significant

performance gain in activities of daily living, motor skills and ambulation.

There is also an additional gain in the gait speed and stride length in these

patients.

Treadmill training can be either speed-dependent treadmill training or limited-

progressive treadmill training. The effectiveness of treadmill training in gait

rehabilitation in PD patients can be explained by the fact that the treadmill

forces the patients to lengthen his or her stride.

Single and Dual Task Training

For gait to be functional in daily life both within the community and home,

people need to be able to dual task. This could involve thinking when walking

or maintaining balance when holding an object. It is well known that

performing an added task interferes with postural stability in older adults

(termed dual task interference) particularly in those adults with impaired

balance.

It is well established that when asked to perform a concurrent task when

walking, people with PD demonstrate reduced gait velocity, step length,

35

increased stride to stride variability and more freezing episodes than when

walking alone. These gait disturbances are also known falls risk factors. An

underlying rationale proposed for dual task interference in PD is that when

required to perform two tasks at the same time, one runs through the frontal

cortical regions and is under conscious control while the other is controlled by

the defective basal ganglia. The task controlled by the frontal lobes is typically

performed with normal speed and amplitude whereas the task controlled by

the basal ganglia may show errors and be under-scaled in speed, amplitude

and force.

Multiple task training in mild to moderate PD has been reported to have

low levels of fatigue, reduced anxiety and high levels of confidence, which

would boost the gait training. The gait tasks undertaken can be progressed

from simple to more complex tasks In addition, a variety of added tasks will be

progressively integrated into the training program. These include tasks such

as listening, speaking, conversing, generation of simple and complex lists,

language, calculation and motor tasks increasing in complexity. Tasks can

include those designed to reflect functional everyday activities such as

carrying bags, getting keys out of a pocket, counting money, recalling

directions or making a shopping list. Complexity will be progressively

integrated as more complex tasks resulting in greater dual task interference

with gait in people with PD.

Step Training

Step training basically consists of walking on the treadmill, supported in a

harness for safety and suddenly turning the treadmill on and off while the

subject stood in the safety of harness either facing forward, backward or

sideways. Step training has been known to result in a reduction of falls,

improvement in gait speed and stride length as well as dynamic balance.

36

Cycling

Cycling is a form of aerobic exercise that may allow the PD patients who

often experience freezing with a new freedom of movement and easy access

to exercise.

Aquatic exercises

It has been proposed that the utilization of an aquatic environment can

promote significant therapeutic results in PD patients such as

(1) a decrease in muscle tone

(2) an improvement of postural stability

(3) an increment of functional mobility

(4) a reduction of spasm severity in spasticity.

The aquatic training protocol can consider simple warm-up exercises, trunk

mobility exercises, postural stability exercises and transitions and change of

body positions.

Virtual Reality

Virtual reality (VR) is defined as “the use of interactive simulations created

with computer hardware and software to present users with opportunities to

engage in environments that appear to be and feel similar to real world

objects and events.” With the advance of technology, VR has been viewed as

a potential rehabilitation tool, because it provides a challenging but safe and

ecologically valid environment, and at the same time is flexible in stimulus

delivery and activity grading. However, it also has some limitations (eg, in-

sufficient depth perception and haptic feedback, and an arbitrary association

between vision and action) that may lead to performances different from those

in physical reality.

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With an appropriate choice of cueing speed, VR is a promising tool for offering

visual motion stimuli to increase movement speed in persons with PD.

Research is needed to examine the long-term effect of VR training that

incorporates target objects moving at appropriate speeds.

Assistive and Adaptive Technology for PD Patients

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We should consider assistive and adaptive technology for those patients

with PD who struggle with functional tasks. These aids can help the patients

maintain maximum function in their day-to-day routines.

Mobility Aids

When a person with PD develops difficulty in balance or walking and has

had a history of frequent falling, it may be time to consider a mobility aid for he

patient. Often a cane is the first consideration to augment the erson’s gait and

increase safety.

When a cane is no longer enhancing mobility and ensuring safety, a walker

is the next choice of aid. Walkers come in various sizes and types and can be

individualized in accordance to the patient’s needs. In extremely severe

stages of the disease or in case of ambulation in the community, a wheelchair

can be recommended for the patient to ease his functional activities.

There are various kinds of technological assistance that can be given to

these patients in terms of modifying simple tasks such as switching on the

lamps to complex tasks like operating a computer. Assistive and adaptive

technology is thus available in a wide spectrum to complement and

supplement a PD patient’s abilities.

Summary

Gait rehabilitation in PD is a comprehensive training program, which needs to

address each and every factor causing gait disturbances in PD patients.

Interventions in the form of specific types of dancing, activities like karate and

boxing or cognitive strategies like mental practice are still in the experimental

stages of their application in PD patients. Gait training forms the most

important aspect of rehabilitation in PD patients as its severity increases and

appropriate and effective strategies can help enhance the quality of life of

patients with Parkinson’s disease.

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