Movement disorders are the hallmark of PD and can severely compromise an individual's ability to perform well-learned motor skills such as walking, writing, turning around, and transferring in and out of bed. According to the American Physical Therapy Association's
Guide to Physical Therapist Practice,
3 the main role of the physical therapist within the multidisciplinary team is to teach people with PD strategies for coping with impairments and disabilities. These strategies, theoretically, will allow them to move more easily, minimize disability, and retain independent living skills. Physical therapists also should be able to assess and measure changes in function, disability, activity, and participation in response to therapy, medication, surgery, and the natural progression of the disease. These roles have been described in detail elsewhere.
3–10 In my opinion, few people initially assessed by physical therapists fit the textbook description of PD,
11 in which the person walks with a forward stooped posture, festinating gait, rigidity, and drooling. In the first 10 years of the disease, I contend, it is more common for people to exhibit slowness of movement, mild gait hypokinesia, resting tremor, micrographic handwriting, and reduced speech volume.
4 In the latter stages, festination, dyskinesia, akinesia, marked hypokinesia, postural instability, and falls are thought to be more of a problem.
11 Because there is considerable variation across individuals in the manifestation of their movement disorders as well as variations in motor performance over time,
4 clinicians should be able to design programs that are tailored to the changing needs of these individuals and their caregivers.
What Is the Nature of the Deficit?
In recent years, there has been a rapid growth in knowledge about the pathogenesis of the movement disorders that occur in people with PD.
12 The most frequently observed movement disorders are described in
Table 1. Of these movement disorders, slowness in the performance of movement sequences (bradykinesia) is the most common and affects around 80% of people with PD.
11Slowness may be so marked as to result in poverty of movement, which is known as “hypokinesia.” People with hypokinesia typically have an expressionless, mask-like face and walk with reduced trunk rotation, short steps, and diminished arm swing, which is more pronounced on one side than the other. Although PD-related movement disorders characteristically occur bilaterally, movement disorders such as bradykinesia are asymmetrical in their severity. This means that physical therapists need to carefully assess the degree of bradykinesia on the right and left sides in addition to comparing their patients' performance with that of people of similar age who are without impairment.
Table 1.
Common Movement Disorders in People With Parkinson Disease
a
All people with bradykinesia experience difficulty in performing repetitive or sequential movements of the limbs such as alternating pronation and supination of the forearms or repetitive tapping of the feet or fingers.
12 This is because movement size progressively decreases during sequential actions. This diminution of movement is known as “motor instability”
13 and can be clearly seen in people with gait hypokinesia, in whom the footsteps become shorter and shorter the further they walk. Likewise, the handwriting of people with PD is typically miniaturized and becomes both smaller and slower as a paragraph is written.
14When a person with PD stops a movement sequence, has a short rest, and begins again, the movement size and speed start at values that are close to normal, then again start to reduce as the new sequence is performed.
There is growing evidence that bradykinesia in people with PD results from disruption of the neurotransmitters used in the neural projections from the internal segment of the globus pallidus of the basal ganglia (BG) to the motor cortical regions known as the supplementary motor area (SMA) and the primary motor cortex.
15 The SMA is critical in regulating the increase in neural activity that needs to occur before a movement is executed.
16,17 It also ensures that a movement is terminated at the appropriate time.
16,17 If the preparation for forthcoming movement is disrupted, then movements can be reduced in size and speed (bradykinesia). At the extreme, if there is no activity in the SMA and primary motor cortex, movement fails to occur.
Absence of movement associated with an inability to initiate movement is known as “akinesia.”
18 Sudden cessation of movement (motor blocks) partway through an action sequence is known as “freezing” (
Tab. 1). Clinical evidence suggests that akinesia and freezing episodes are context dependent.
18 For example, the person may “freeze” when attempting to walk through a narrow doorway or when making a transition from walking on carpet to wooden floorboards, even though he or she can walk quickly without motor blocks across an empty parking lot. Research on primates suggests that spiny neurons in the striatum of the BG play a role in recognizing patterns of input from convergent input from multiple cortical sites.
19This recognition of behavioral events or environmental contexts from prior experience may then be used for the planning and performance of intelligent behavior.
20 It has been hypothesized that when striatal pattern recognition is defective, motor performance is not ideally matched to task demands.
Some people with PD can also find it difficult to cease actions such as walking, turning around, or speaking,
21 presumably because they have sustained discharge in the SMA, rather than the rapid drop in neural activity in the SMA that normally allows movements to be terminated. Difficulty terminating locomotor actions such as walking, running, or turning during walking is thought to be one of the major factors that predisposes people with PD to slips, trips, and falls.
22
The neurotransmitter imbalance in the motor cortex-BG-motor cortex feedback loop arises due to a relentless and progressive death of neurons in the substantia nigra pars compacta (SN) of the brain stem.
15 These brainstem neurons normally secrete the neurotransmitter dopamine that apparently plays a role in allowing people to execute well-learned skilled movements quickly and smoothly. Why cell death occurs in this region of the brain stem is not known, although exposure to environmental toxins coupled with a genetic predisposition to PD is one hypothesis.
23 What is known is that the balance of dopamine, gamma-aminobutyric acid (GABA), enkephalin, glutamate, acetylcholine, and substance P in the BG is normally very finely tuned.
15 In people with bradykinesia, there is a decrease in the excitation of the dopaminergic projections from the SN to the striatum and the internal globus pallidus coupled with a reduction in the inhibitory activity of dopaminergic projections from the SN to the striatum and the external globus pallidus.
15 The net result is excessive inhibitory output from the globus pallidus to the thalamus that leads to reduced movement. In contrast, with Huntington disease, for example, there is a progressive loss of GABA/enkephalin neurons in the striatum that project to the external globus pallidus, and as a result large-amplitude, irregular, involuntary choreiform movements occur.
24
In a similar way, some people with advanced PD who have been receiving levodopa medication for more than 15 to 20 years develop dyskinesia, which may be associated with relatively excessive amounts of GABA/ enkephalin. Dyskinesia manifests as purposeless wriggling or writhing movements as well as dystonic posturing of the feet, hands, trunk, and neck. This condition includes chorea, athetosis, tics, dystonia, and tremor.
22 The term “dystonia” refers to excessive and sustained overactivity of a particular muscle group such as the triceps surae or long finger flexors. The overactivity occurs for periods of minutes to hours and frequently recurs over the course of a day, month, or even years.
Dyskinetic movements are usually most noticeable when a person is sitting upright, standing, or walking, and they disappear when the person is asleep. Dyskinesia can be categorized according to the following characteristics:
peak dose: typically occurs 1 to 3 hours after medication is taken
biphasic: peaks twice within the levodopa medication cycle, typically in the half-hour periods at the beginning and end of the dose
end of dose: commences around 30 minutes prior to the next dose
nocturnal: occurs only at night time when medication levels are low
random presentation
Bradykinesia, akinesia, freezing, and dyskinesia are not the only movement disorders in PD. As early as 1967, Martin
25 recognized that balance disorders were also an inherent feature of the disease. The reason why balance is disrupted is unclear, although it appears to be associated with neurotransmitter disturbances in the output projections from the internal globus pallidus to the midbrain and brain-stem regions involved in maintaining upright stance and extensor muscle activity.
21 A balance disturbance in a person with PD is most easily detected by quickly and unexpectedly pulling the person backward at the shoulders while he or she is standing with his or her feet slightly apart.
26 People without PD respond to this “pull test” by dorsiflexing their ankles, lifting the arms forward, and, in some cases, flexing forward at the hips. When the pull is stronger, individuals without PD typically take a step backward to protect them from falling. In people with PD, these postural responses are compromised, and the ankle, hip, arm, and stepping strategies are either absent or diminished in amplitude.
27 They might take several steps backward to recover stability or, in more severe cases, fall rigidly into the therapist's arms. People with a balance disturbance of this type are at high risk for falls. This is particularly the case when they have to respond to an unexpected push or pull or an unexpected movement of the support surface they are standing on, or when they have to make automatic postural adjustments.
27
Another hallmark of idiopathic PD is rigidity.
28 Rigidity can be detected by slow passive movement of the affected body part while the person focuses his or her attention on a secondary task (such as reciting the days of the week backward to avoid compensating for his or her movement disorder). The examiner assesses the degree of resistance encountered while passively moving the affected body part. The resistance is either “lead pipe” (slow and sustained) or “cogwheel” (where tremor is superimposed on rigidity). There is some evidence that rigidity is due to abnormal activation of long-latency stretch reflexes coupled with an increase in central reflex gain.
28 In addition, muscle stiffness is increased in people with advanced PD due to changes in the peripheral mechanical properties of muscle.
29Although the effect of rigidity on passive movement can be detected, the neural component of rigidity does not appear to compromise voluntary movement.
17Moreover, people with PD rarely complain about its presence, even when a clinician rates it as severe.
22 For these reasons, there appears to be little point in directing physical therapy treatment toward reducing the neural component of rigidity, as was suggested in the 1950s and 1960s.
30 A controlled trial of physical therapy using proprioceptive neuromuscular facilitation, the Bobath technique, and the Peto method (a method of conductive education) to reduce rigidity and increase rotation showed these interventions were ineffective in enhancing walking, decreasing festi-nation, or increasing range of movement.
31
Resting tremor (4–6 Hz) is also characteristic of idiopathic PD and is often the first symptom reported.
11 It may be due to an altered firing rate of thalamic neurons, although the exact mechanism by which this occurs is not known. Less commonly, action tremor (6–8 Hz) can be observed during the execution of movements, or postural tremor can be observed when the person bears weight through the limb or encounters resistance to movement of the limbs, trunk, head, or neck.
11Physical therapists rarely need to treat individuals with resting tremor because it disappears during movement and therefore does not interfere with the ability to perform everyday tasks such as walking, writing, or grasping objects. In addition, resting tremor responds well to levodopa. There are anecdotal reports
32 that physical therapy interventions such as relaxation and directing attention toward minimizing tremor may have short-term beneficial effects on the severity of resting tremor. However, these effects are only transient.
32 Tremor severe enough to be considered socially unacceptable by the person with the disease, in my opinion, may be best treated by surgical interventions such as thalamotomy, pallidotomy, and deep brain stimulation.
A Model for Physical Therapy
One of the striking features of PD is that the ability to move is not lost, rather there is an activation problem.
13,25 As a result, people with PD appear to be reliant on cortical control mechanisms to initiate movement.
8,13,19,20,25 There is also evidence of increased reliance on frontal-cortical “attentional” mechanisms to sustain the execution of complex movements, due to defective BG mechanisms subserving movement automaticity.
13,16,17,25 The current model for physical therapy intervention in people with PD is based on the assumption that normal movement can be obtained by teaching patients strategies to bypass the BG pathology. The Figure illustrates the factors taken into account when this model was created and for setting the conditions for training. When planning physical therapy interventions, I believe that therapists should take into account the response of movement disorders to external cues and attentional strategies, knowledge of how interventions can be adapted according to severity of cognitive impairment, the need to analyze functional task performance as a basis for designing task-specific training regimens, and the effects of PD medication on movement. In addition, when designing training programs tailored to the needs of individuals and their caregivers, I contend that physical therapists need to consider the effects of aging, concurrent pathologies, and secondary adaptive changes in the musculoskeletal and cardiovascular systems (
Figure).
Figure.
Key elements of the model for training people with Parkinson disease to utilize strategies for performing functional motor tasks.
Knowing about the characteristic features of movement disorders in people with PD is, in my opinion, the starting point for designing physical therapy interventions. Despite the troublesome nature of disorders such as hypokinesia, akinesia, and dyskinesia, people with PD have a remarkable capacity to move quickly and with near-normal movement size under certain circumstances.
33–37For example, when a person with PD performs a simple ballistic task such as pointing to an object or catching a moving ball, the movement size and speed are frequently normal.
33 However, when simple movements are integrated into a long or complex action sequence, they are performed slowly and with much more difficulty.
34 This is presumably because the primary motor cortex, brain stem, and spinal cord are the major anatomical regions involved in the control of simple, ballistic or reflexive movements, whereas more complex actions are regulated by the cerebellar circuits and cortex-BG-cortex feedback loop.
13 The latter is defective in people with PD.
13 Notwithstanding this, performance has the potential to be enhanced by training people with PD to break down long or complex sequences into component parts and to focus their attention on performing each part separately.
32 People with PD also benefit from focusing their attention on performing one task at a time and avoiding dual task performance.
8,38Presumably, when 2 activities are performed at the same time, one activity is controlled by the faulty BG while attention is focused on the other activity, and the task that runs through the BG reduces in speed and size.
8 Preparing in advance for forthcoming movement by using mental rehearsal and visualization might also be of benefit,
32 although the effects of these strategies have not been documented through controlled clinical trials.
Evidence is accumulating that people with PD can move more easily when external cues are available to guide their performance.
35–37 External cues can be visual, auditory, or proprioceptive in type. For example, when people with gait hypokinesia are provided with visual cues on the floor set at the appropriate step length for their age, height, and sex, they are able to walk at normal footstep amplitude and speed, provided they do not have severe postural instability.
35–37 In a similar way, lined paper assists people with micrographia to write with larger strokes.
14 Auditory cues appear to be particularly useful for people with gait akinesia and freezing, whereas visual cues are most useful for people with gait hypokinesia.
35–37 Rhythmical sensory cues, such as rocking the body from side to side, may sometimes be useful in assisting the initiation of movements such as walking or rolling over in bed.
10 External cues may assist people with PD to move more easily because they utilize the intact premotor cortex of the brain rather than the defective BG-SMA circuits to control movement.
39 An alternative explanation is that external cues may simply focus the person's attention on critical aspects of the movement that need to be regulated, such as stride length,
35–37 weight transference to unload the leg, or axial motion to assist in turning.
6 Both of these explanations are compatible with the idea that the ability to move is not lost in people with PD, rather the person is dependent on cortical mechanisms to activate and sustain movement.
The presence of external cues is not mandatory for activating neuronal networks in people with PD. In people who are cognitively intact, simply focusing attention on the critical aspect of movement that needs to be controlled can be sufficient to activate movement with near-normal speed and size.
37,40–42 Because cortical regions remain unaffected by the disease in the early stages, the person appears to be able to use “online” frontal-lobe cognitive strategies to compensate for BG insufficiency. Strategies that rely solely on methods such as these, however, may not be effective in people with severe cognitive impairment due to the accumulation of inclusion bodies (Lewy bodies) in neurons throughout the cortical, subcortical, and brain-stem regions in individuals with end-stage PD.
43 Because Lewy bodies impair mitochondrial processes,
23 neural function throughout large regions of the central nervous system becomes compromised. The implication for physical therapy is that training that relies on cortically mediated learning processes and cognitive strategies may not be effective in people with end-stage PD because the capacity for learning new motor skills declines.
42 People with cognitive impairment might well benefit more from external cues, environmental restructuring, and demonstrations or instructions from physical therapists and caregivers, as these strategies appear to be less reliant on complex information processing.
Task analysis and task-specific training are central elements of the model (
Figure). In my opinion, knowledge of the biomechanics of movement for a range of everyday tasks can be used in an attempt to ensure that the most efficient strategy is taught. Researchers who have measured biomechanical performance in people with PD in response to different physical therapy treatment strategies have provided data that clinicians might find useful.
24,37,40,44 I further argue that it is important for training to take place within the context of functional tasks of everyday living, such as walking, standing up from a sitting position, turning around, moving around the bed, writing, and dressing. Task-specific training seems, in my view, particularly appropriate, given that movement disorders appear to be context dependent
19 and are most prominent for well-learned, complex motor skills.
33,34 Although there has not yet been a controlled clinical trial comparing the effects of training functional motor tasks with the effects of training isolated movements, the motor skill learning literature indicates that generalization of training is most effective when there is a high degree of similarity between the trained task and new variations of the task.
45 From my perspective, there is little point, for example, in training a person to control dystonia in the foot while lying supine if the training does not generalize to walking, standing up, or obstacle negotiation. It is preferable to train the person to control dystonia while walking, as this is when it is much more disabling.
To further enhance transfer and retention of training, I suggest that physical therapy takes place in the environment where the individual's movement disorders are most troublesome. This is usually inside the person's home, in the bedroom, bathroom, kitchen, or family room, although training the person to use community ambulation skills such as road crossing and negotiation of obstacles (eg, curbs) is frequently also a priority. If the physical therapist is unable to travel to the person's residence, then key aspects of the home environment can be simulated in the physical therapy department so that the person can practice the movement strategies in a similar context. Environmental modifications such as creating open walkways and providing ramps and rails to optimize movement and reduce the risk of falls in people with PD should be considered. However, controlled clinical trials are needed to measure the effects of environmental context on motor performance in people with PD.
The effects of PD medications on movement and functional capacity should not be overlooked (
Figure).
4,5,46 In the early stages after diagnosis, patients can have an excellent response to drugs such as levodopa and apo-morphine and show very little residual deficit.
11 However, after a number of years, movement disorders again become commonplace, and motor performance can become highly variable.
4These variations in performance are known as “motor fluctuations.” For this reason, physical therapists need to ensure that they train people with PD to cope with movement disorders during both “off” and “on” periods of levodopa use. The “off” phase is when levodopa levels are low and movements are hypokinetic, typically at the end of the levodopa cycle. The “on” phase is usually at peak dose, when movements are more normal. I contend that, at times, this will necessitate 2 different sets of strategies—one set of movement strategies for when they are at the end of a dose and very hypokinetic and another set of movement strategies for when they are at peak dose and have a different combination of movement disorders.
22,26 For people who have uniphasic, biphasic, peak-dose, end-of-dose, or random presentation dyskinesia, training needs to focus on strategies for coping with the involuntary extra movements whenever they occur during the medication cycle. Moreover, clinical observations suggest that it is advisable for people to perform activities to maintain general strength, range of movement, and fitness as well as task-specific training when they are at peak dose during the medication cycle.
22 For example, the daily routine can be planned so that walking or playing golf occur from 11
AM to 1
PM or from 3 to 5
PM if they are on the typical levodopa schedule where medication is administered at 6
AM, 10
AM, 2
PM, 6
PM, and 10
PM.
Aging, concurrent medical conditions, and secondary adaptive changes in the musculoskeletal and cardiovascular systems, in my view, are also important considerations when devising the physical therapy program. The majority of people with PD are older than 65 years, and many have age-related frailty or concurrent medical conditions and lead a sedentary lifestyle.
32 People with PD, therefore, are at risk of developing weakness, reduced joint range of movement, thoracic kyphosis, and diminished aerobic capacity because they tend to reduce the amount and variety of physical activities they perform.
32 They can also experience reductions in exercise capacity
47,48 and can have diminished force production.
49,50 Shortening of the triceps surae muscle is also a frequent outcome of prolonged hypokinesia
10 and limits power generation at the ankle at the end of the stance phase of gait.
51 The physical therapy assessment needs to differentiate between movement disorders that are due to PD and those that arise from other conditions or disuse (this process is discussed in detail elsewhere
4,9). Physical therapy treatment can then be tailored to the specific movement disorders found on assessment.
9,10,32
Finally, I suggest that, to obtain the full benefit of physical therapy intervention, the perceived needs articulated by the patients and their caregivers and utilization of the diverse skills of the multidisciplinary team need to be taken into consideration (
Figure).
52 Because PD progresses slowly, patients and their families need to be consulted in developing programs to be implemented over the long-term. This consultation will assist them in taking greater responsibility for the management of their health and well-being.
9,10 The wide range of motor, cognitive, autonomic, and psychosocial problems that can occur in people with PD may be too complex for any single practitioner to manage in isolation.
52 In this regard, the ability of the physical therapist to consult with other health care professionals with specialist skills would appear to be a distinct advantage.
Case History: Mrs A
In 1988, at the age of 39 years, Mrs A was diagnosed with PD by her family general practitioner after exhibiting a mild resting tremor of her left hand, micrographia, slowing of movement, and occasional loss of balance. Mrs A had previously been well and lived at home with her husband and 16-year-old daughter. She reported home duties as her occupation. Because the movement disorders were initially mild, the general practitioner advised that drug treatment be withheld until symptoms were more apparent. By 1990, Mrs A reported that domestic tasks were becoming increasingly difficult to perform due to slowness of movement, tremor, and loss of balance. She was referred to a neurologist, who prescribed Madopar M
†(levodopa benserazide) to be taken 5 times per day, and this medication provided temporary relief of all symptoms (
Tab. 5).
Table 5.
Physical Therapy Assessment Data for Mrs. A Over a Period of 10 Years
a
By April 1993, the symptoms had re-emerged due to disease progression, despite attempts to adjust medication. Mrs A was referred to the Kingston Centre Movement Disorders Clinic for consultation with the physical therapist, neurologist, occupational therapist, and other team members. Over the first 3 clinic consultations (spaced 1 month apart), the physical therapist conducted an assessment of movement disorders and functional disability and commenced a movement training program. The initial physical therapy assessment in May 1993 revealed the following problems:
a short-stepped hypokinetic walking pattern,
mild gait akinesia and occasional freezing in doorways,
delayed stepping response to external perturbation of the center of mass in steady stance, and
moderately severe resting tremor of the left (non-dominant) hand.
In addition, at the end of dose of each 4-hour medication cycle, there was moderately severe dyskinesia of the head, upper limbs, and trunk. The episodes of dyskinesia were most pronounced in the afternoons, particularly around 3:30. Due to the dyskinesia, driving was restricted to the mornings. The neurologist, therefore, changed the medication regimen by adding Madopar Q
† 5 times a day to the Madopar M that Mrs A was already taking.
Because Mrs A attended the clinic as an outpatient, the physical therapy intervention consisted of a home program to overcome movement difficulties. The physical therapist and the occupational therapist attended the home in an attempt to ensure that strategies were being used effectively in that setting and were reinforced by the family. An outdoor mobility course was mapped out in the back garden to enable Mrs A to practice maintaining balance during locomotion. Homework (a home practice routine) was written up in a diary and included strategies for coping with gait hypokinesia (visual cues and attentional strategy training), freezing (counting out loud, rhythmically rocking from side to side, stopping the task and then beginning the task again, and thinking of stepping over a log), postural instability (practicing stepping strategies, mobility course), and extra movements (looking at the part that is moving excessively and thinking about reducing the overactivity of that part; progressive relaxation). For general fitness, she was encouraged to continue with daily half-hour walks and twice-weekly yoga classes. In addition, the physical therapist together with the other team members commenced the process of educating Mrs A and her family about PD and how to best cope with movement disorders. Information was also provided on how to access support groups, such as the Parkinson's Disease Association.
The next contact was in June 1994 when Mrs A was admitted to the inpatient ward for a 3-week period to monitor the effects of medication and provide her with an opportunity for intensive movement training. The main problems noted by the physical therapist at the admission assessment were:
painful dystonic posturing of the left foot due to overactivity of the gastrocnemius and soleus muscles during walking and standing tasks,
difficulty rolling over to the left and getting out of bed,
reduced left-hand dexterity, limiting the ability to sew, prepare food, and tie laces, and
difficulty writing in the afternoons and evenings.
The goals of physical therapy were modified to include: (1) teaching Mrs A additional strategies for overcoming dystonia, (2) enhancement of bed mobility, and (3) use of visual cues and attentional strategies for improving writing and dexterity of the hands. To temporarily reduce dystonia, Mrs A was shown how to perform a prolonged stretch of the gastrocnemius and soleus muscles in standing. In an effort to enhance bed mobility, she was taught to mentally rehearse the rolling-over sequence, read instructions on a cue card placed on a bedside table, and break the action of rolling over into parts. Mrs A was also trained to deliberately look at the object she was reaching for and to practice a variety of upper-limb tasks, as outlined in
Table 2. While an inpatient, Mrs A attended two 40-minute physical therapy sessions 5 days a week for the 3-week period. Over this time, she made considerable gains, and at the time of discharge she was using stretches to temporarily overcome the dystonia. Her stride length had increased, and she was able to walk more than 200 m at a time by concentrating on walking with large strides. Upper-limb performance was functional.
Mrs A returned home with her diary revised to include gastrocnemius and soleus muscle stretches, bed mobility activities, and use of attentional strategies during upper-limb performance in addition to the other tasks. She was re-examined at 6 monthly intervals at the Movement Disorders Clinic. She remained stable until July 1996, when she experienced a series of falls. Readmission to the inpatient ward for assessment and reinforcement of movement training was arranged. On admission, mild bradykinesia was evident. During the previous 6 weeks, she had fallen in the garden when weeding, had slipped on the bathroom mat and fallen to the floor, and had fallen again in the garden when turning around to talk to her grandson. There was no evidence of postural hypotension. The physical therapy assessment showed that she could maintain steady standing positions with feet apart, with feet together, during stride stance, and during single-limb stance for the maximum testing time of 30 seconds. However, she performed poorly for her age on the step test and the Pastor Pull Test.
26
Physical therapy intervention at this stage was targeted at preventing falls. In addition to reinforcing the need to focus attention on maintaining balance when performing mobility tasks in a standing position, she was educated about the risk factors for falls. Another home visit was conducted by the physical therapist and the occupational therapist, with Mr and Mrs A present. This home visit resulted in the removal of loose mats, cords, and a glass-topped coffee table in the center of the family room. The occupational therapist recommended that the concrete path in the back garden be repaired, and a set of handrails was installed at the backdoor steps. A rail was also installed in the shower recess, and a nonslip mat, shower chair, and handheld shower hose were provided for showering. Mrs A was encouraged to maintain regular physical activities, such as walking and yoga, with a partner present. She was provided with a falls diary and trained in how to record the date, time, location, and perceived reason for each fall. After discharge, Mrs A continued with 3 monthly monitoring visits to the Movement Disorders Clinic and continued with the daily homework program and falls diary.
In February 1998, Mrs A was again admitted to the inpatient ward, this time for severe resting tremor in the hands at the end of dose. The neurologist hypothesized that the tremor was due to neurotransmitter imbalance, and her medication regimen was therefore altered to levodopa carbidopa and pergolide (
Tab. 5). Before and after alteration of the medication regimen, the physical therapist conducted dose-response trials, which are serial measurements used by physical therapists, to chart the effects of medication on movement disorders and independence (refer to Morris et al
5). The new medication regimen soon ameliorated the tremor and resolved residual dexterity problems of the left hand. However, mild gait hypokinesia was again apparent. With longer walking sequences, the walking speed slowed even further, and she was finding it difficult to traverse pedestrian crossings with sufficient speed to avoid traffic. Although Mrs A only took 10 seconds to complete the Timed Up & Go Test,
79 her footsteps progressively reduced in size and number of steps during the turning component of the test.
The goals of physical therapy at this stage were to increase her walking speed to 75 m/min and to teach her strategies for avoiding motor instability when walking and turning. Once again, training incorporated the use of mental rehearsal (visualizing walking with long steps before the action), visual cues and attentional strategies, avoidance of secondary task performance when walking and turning, and turning using a large, “whole-body” arc of movement rather than swiveling around on a small base of support. Training was conducted within the context of community ambulation tasks such as road crossing, shopping, and negotiation of curbs, slopes, and rough ground. To continue to promote general fitness and aerobic capacity, Mrs A was encouraged to walk for 30 minutes each day with another person, as well as to continue with her regular yoga classes. By the end of this 3-week admission, Mrs A had achieved her major goal of walking confidently at 75 m/min over a range of surfaces as well as having no residual tremor or difficulties with reaching, grasping, and manipulating objects. She again was discharged home with a home program written up in her diary.
When Mrs A was re-examined in December 1998, micro-graphia, mild bradykinesia, and dystonia of the plantar flexors were found to be residual problems that were not markedly disabling. Because her aerobic capacity and walking distance had diminished, these problems become the focus of a burst of more intensive physical therapy treatment. She was encouraged to walk at least 3 times a week, concentrating on maintaining long strides, and to participate in yoga and other physical activities.
This case history illustrates how physical therapy intervention was adapted according to the client's needs over the first 10 years that she had PD. The example shows how the signs and symptoms of PD as well as the medication regimen changed over time, requiring frequent adjustment of physical therapy goals and procedures. Some problems persisted, despite attempts at adjusting medication and physical therapy. The persistent problems were dystonia of the gastrocnemius and soleus muscles, micrographia, postural instability, and mild gait hypokinesia. The most intensive period for physical therapy was in May 1993, when the initial medication regimen and physical therapy training program needed to be established. For this woman, bursts of goal-directed physical therapy provided within a multi-disciplinary team setting appeared to be particularly helpful in managing the symptoms of PD.
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