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 4

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 8

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. 10

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-Omethyltransferase 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 17

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 3dimensional 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

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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 33

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 limitedprogressive 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,

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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.

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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, insufficient 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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