The role of the physiotherapist in quantifying movement fluctuations in Parkinson's disease

ORIGINAL ARTICLE

Meg Robert~a!i1sek

Although a variety of medications are used in the treatment of Parkinson's disease, all have short term effects. As a result, motor performance varies over time. A key role of the physiotherapist is to measure fluctuations in the severity of movement disorders in relation to the dose and timing of anti-Parkinsonian medication with a view to: (i) optimising motor performance; (ii) targeting therapeutic interventions for times of greatest need; and (iii) communicating findings to the interprofessional team. For an informed approach to the measurement of medication-induced motor fluctuations, clinicians require an ur.derstanding of the pathophysiology of Parkinson's disease, the mode of action of medications and the validity of existing methods used to quantify changes in performance resulting from pharmaceuticals and rehabilitation. [Morris M. lansek Rand Churchyard A: The role of the physiotherapist in quantifying movement fluctuations in Parkinson's disease. Australian Journal of Physiotherapy 44: 105-114]

Key words: Parkinson Disease; Medication Systems; Movement Disorders; Physical Therapy M Morris BAppSc(Phtyl, GradDip(Gerontl. MAppSc, PhD is Managerofthe Geriatric Research Unit at the Kingston Centre, Melbourne, and Adjunct Associate Professor in the School of Physiotherapy at La Trobe University. Robert lansek PhD, FRACP is Director of the

The role of the physiotherapist in quantifying movement fluctuations in Parkinson's disease

arkinson's disease is a chronic neurological condition that leads to a progressive decline in motor performance as well as cognitive impairment. It affects at least 1 per cent of people over 75 years of age (Schoenberg 1987). Therefore it can be estimated that more than 30,000 Australians currently suffer from Parkinson's disease. With the rapid population ageing throughout industrialised countries, there has been a sharp increase in the demand for effective medical and physiotherapy services for people with this disabling condition. ·Because the cause of Parkinson's disease is not yet known, treatment is currently symptomatic. The disease affects the ability to perform welllearned movement sequences such as walking, writing, reaching and grasping, dressing and swallowing, hence treatment aims to reduce the severity of movement disorders that compromise these functions. The classic movement disorders that are observed in people with Parkinson's disease are:

•

hypokinesia - reduced movement speed and amplitude (poverty of movement); • akinesia - difficulty initiating movement; motor blocks during movement; • tremor - usually resting tremor although can present as postural tremor; • rigidity - increased stiffness which can be detected during passive movement testing; • postural instability - defective proactive and reactive balance control mechanisms; and • dyskinesia - involuntary extra movements including chorea and dystonia which occur in end-stage disease. These movement disorders arise due to a progressive loss of neurones in the substantia nigra located in the midbrain that normally produce the neurotransmitter dopamine. Dopamine is used in conjunction with other neurotransmitters to enable the basal ganglia to control movement. As illustrated in Figure 1, the basal

Movement Disorders Program at the Kingston Centre and Professor of Geriatric Neurology at Monash University. Andrew Churchyard PhD, FRACP is a neurologist at the Movement Disorders Program at the Kingston Centre.

Correspondence: Associate Professor Meg Morris, Manager Geriatric Research Unit, Kingston Centre, Warrigal Rd, Cheltenham, Victoria 3192.

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Table 1. Medication used in the treatment of Parkinson's disease*

Generic Name

Type of Drug

Aim

1. Dopamine Precursors

Dopamine replacement therapy: boosts the production of dopamine in remaining substantia nigra cells

Levodopa carbidopa

Mimic or replicate the action of dopamine by stimulating Dl or D2 receptors in the striatum

2. Dopaminergic Agonists

3. Anticholinergics

Reduce the relative increase in acetylcholine in proportion to dopamine in the basal ganglia

Example of Brand Names

Potential Side Effects

Levodopa benserazide

Sinemet Kinson Madopar

Nausea Light headedness Confusion Hallucinations Paranoia

Apomorphine Cabergoline

Apomorphine Cabergoline

Bromocryptine Mesylate

Parlodel Kripton

Nausea Vomiting Confusion Postural hypotension Hallucinations

Pergolide Mesylate Lysuride

Permax Lisuride Visual disturbance Cognitive impairment Confusion and hallucinations in elderly people Urinary retention Dry mouth

Benzhexol Hydrochloride Orphenadrine Hydrochloride Benztropine Mesylate Procyclidine Hydrochloride

Artane Akineton Disipal

Amantadine Hydrochloride

Symmetrel

Urinary retention Ankle oedema Dizziness Confusion and hallucinations in elderly people Orthostatic hypotension

Deprenyl Eldepryl

Nausea Vomiting Postural hypotension Confusion and hallucinations

4. Adamantane Derivatives

Enhance the action of levodopa; glutamate blockers; may offer neuroprotection

5. MAOB Inhibitors

Enhance the action of Selegiline levodopa; block the Hydrochloride breakdown of dopamine. May reduce the rate of loss of substantia nigra cells (neuroprotective effect)

Cogentin Kemadrin

*Adapted from Reynolds EF (1996): The Extra Pharmacopoeia. (31 st ed.) London: The Pharmaceutical Press

ganglia are a group of subcortical nuclei located deep within the brain. They are comprised of the substantia nigra, the caudate nucleus and putamen (together known as the

striatum), the globus pallidus and the subthalamic nucleus. The putamen and postero-ventral globus pallidus form the motor part of the basal ganglia, whereas the caudate nucleus and the

antero-dorsal globus pallidus play more of a role in cognition (DeLong 1993). The major input projections to the basal ganglia are the motor and non-

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Table 2. Long and short acting levodopa preparations

Generic Name

Short Acting Preparation (Brand name)

Long Acting Preparation (Brand name)

Other Preparations Liquid Levodopa

Levodopa carbidopa

Sinemet 100125 Sinemet 25012 5 Sinecarb 100110 Sinecarb 100125 Sinecarb 250125 Kinson 10012 5 Madopar 200/50 Madopar M 10012 5 Madopar Q 50/12.5

Sinemet M 100/10 Sinemet CR 200/50

(Sinemet 100125 or Kinson 10012 5 dissolved with ascorbic acid mixed into solution with water)

Levodopa benzeraside

motor areas of the cerebral cortex and the thalamus. The major output projections are via the thalamus to the motor cortical regions such as the supplementary motor area, premotor area and primary motor cortex (Iansek et alI995). Figure 1 illustrates the cortico-basal ganglia-cortex motor loop which regulates the performance of motor skills. Within this feedback loop there are two motor circuits (Alexander and Crutcher 1990). The "direct" pathway travels from the putamen to the internal globus pallidus, substantia nigra pars reticulata and then the thalamus. The "indirect" pathway travels from the putamen to the external globus pallidus and subthalamic nucleus before reaching the internal globus pallidus, substantia nigra pars reticulata and thalamus. Normally there is a delicate balance between the activity of the direct and indirect pathways which allows movements to be performed smoothly, quickly and easily. In Parkinson's disease it is thought that under-activity of the direct pathway leads to hypokinesia whereas over-activity of the indirect pathway is associated with dyskinesia. The basal ganglia utilise a range of different neurotransmitters to regulate movement. Dopamine is manufactured by substantia nigra neurones and binds to and activates D1 and D2 receptors in the striatum (Figure 1). Within the striatum, GABA is a major neurotransmitter for the striatal

Madopar HBS 100125

GABA Dyn()tplili:l

SubSta1ice P

GP/SNpr

(Inhibitory)

Figure 1. Basal ganglia motor loop involved in the control of complex movement sequences. Sf\lpr - substantia nigra pars reticulata; Sl\Ipc - substantia nigra pars compacta; Gile - globus pallidus exterrms; GP j - globus pamdus interims; STN - subthalamic nucleus. Adapted from Delong (1993, p.6) (Figure 1), ill Memo 1\1, Hamada i, lJel..01l9 ME: Role of cerebellum and basal ganglia in voluntary movement, with kind permission from Elsevier Science, Amsterdam.

projection neurones, although dynorphin, substance P and enkephalin co-localise with GABA in the striatal projection neurones. Acetylcholine is a neurotransmitter used by interneurones. It is thought that a relative excess of acetylcholine in comparison with dopamine is critical in creating symptoms of Parkinson's disease (Nutt 1987). The pathway from the subthalamic nucleus to the internal globus pallidus and substantia nigra is mainly activated by glutamate (DeLong 1993). People with Parkinson's disease typically have a cluster of neurotransmitter disturbances which include a marked reduction in dopamine together with a relative increase in acetylcholine and glutamate. Because Parkinson's disease is progressive, loss of dopamine producing neurones in the substantia nigra continues over time. The reason why this progressive cell death occurs is currently not known. One possible explanation is that oxidation of the cell membranes and mitochondria of substantia nigra neurones occurs due to an excessive accumulation of free radicals in the brain (Youdim and Riederer 1997). Free radicals are large molecules that have an unpaired electron. It is hypothesised that they acquire electrons from cellular structures in the substantia nigra, leading to oxidation and cell death (Youdim and Riederer 1997). Despite the use of medications such as

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Table 3 continued.

Test

Investigators

Reliability and Validity

•

Passive movement Visual observation Steady Stance Tests: feet apart; feet together; single limb; tandem; step stance Proactive control: arm raises, step test, functional reach Reactive control: sternal push Pastor test Visual observation

Not reported Not reported Smithson et al (1998); Hill et al (1996a and 1996b)

Not reported Not reported Retest reliability confirmed for steady stance tests, functional reach and Pastor test (Smithson et al 1998) and for elderly and stroke subjects (Hill et al 1996a and 1996b)

•

•

•

Rigidity Tremor Postural Instability

Dyskinesia

levodopa to redress neurotransmitter imbalances, cell death in the substantia nigra continues. Eventually, in patients with end-stage disease, insufficient cells remain in the substantia nigra which are able to convert levodopa to dopamine; the duration of the response to levodopa shortens and motor fluctuations develop. Motor fluctuations are unpredictable changes in movement characterised by periods of akinesia and hypokinesia interspersed with bouts of dyskinesia (Iansek et al 1997). The unpredictable response to levodopa makes management difficult for the physician and frustrating for the patient. For these reasons, physiotherapy is usually provided in conjunction with medication, to teach people strategies to move more easily when motor fluctuations inevitably occur.

Parkinson's disease medications Medications used in the treatment of movement disorders in Parkinson's disease can be categorised into five major groups, based on the neurotransmitter imbalances they target and their role in preventing cell death (Table 1). These include medications that: (1) boost the production of the neurotransmitter dopamine;

Smithson et al (1998)

Pastor et al (1996) Dyskinesia subsection UPDRS Iansek (1997) refer to Morris, Churchyard and Iansek (1998)

(2) mimic the effects of dopamine by stimulating dopamine receptor sites in the striatum; (3) reduce the acetylcholine imbalance in the striatum; (4) block over-activity of the neurotransmitter glutamate; and (5) p:ovide protection for substantia mgra neurones. (1) Drugs that boost the production of the neurotransmitter dopamine Levodopa preparations such as levodopa-carbidopa (Sinemet, Kinson) and levodopa-benserazide (Madopar) p'rovide the mainstay of pharmacological treatment for Parkinson's disease. Levodopa is converted into dopamine by dopadecarboxylase in the brain, blood, gut, liver and muscle. Dopamine cannot be used directly by the basal ganglia, as it cannot cross the blood-brain barrier and is metabolised in peripheral regions such as the liver. In contrast, levodopa is able to cross the walls of selected blood vessels that allow transport of chemicals to the central nervous system (CNS), and then is converted to dopamine by viable substantia nigra cells (Cotzias et al 1969). The high dose of levodopa forces substantia nigra neurones to increase production of dopamine. Microglia and to a lesser extent astrocytes in the striatum can also

Not reported

convert levodopa into dopamine. Levodopa preparations always include a peripheral decarboxylase-inhibitor (such as carbidopa or benserazide) to minimize metabolism of this compound in the periphery. To help control for shortened drug effects, controlled release preparations of levodopa such as Sinemet CR and Madopar RBS are now available that provide moderate stabilisation of plasma levodopa levels and have longer lasting effects (Table 2) (Nutt 1987). Levodopa provides good symptomatic relief for approximately 5-8 years (Jankovic and Marsden 1988). After that time, it becomes less and less effective; the response amplitude remains the same although the duration of the effect shortens. This is due in part to fewer cells available in the substantia nigra to covert levodopa into dopamine. (2) Dopamine agonists Dopamine agonist drugs mimic the action of dopamine by directly stimulating the Dl and D2 receptor sites in the striatum. They are also thought to boost the uptake of dopamine in the striatum by stimulating presynaptic receptors (Jankovic and Marsden 1988). Most frequently used are the D2 agonists bromocryptine (Parlodel, Kripton) and pergolide (Permax).

•

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Apomorphine is used in those people with severe motor fluctuations arising from Parkinson's disease. It acts as a dopamine agonist on both the D 1 and D2 striatal receptors (Metman et al 1997) and is prescribed in conjunction with domperidone in order prevent nausea and vomiting. Apomorphine is administered parentally with a continuous infusion pump or by subcutaneous injection. Subcutaneous apomorphine takes approximately 5-10 minutes to take effect and lasts for around 90 minutes. (3) Drugs that reduce the activity of acetylcholine within the striatum

As early as 1867, physicians had noted that patients with the "shaking palsy" showed some improvement in resting tremor when they ingested extracts from the belladonna nightshade plant (Jankovic and Marsden 1988). This extract was later found to contain anticholinergic agents which inhibited the relative over-activity of acetylcholine in the striatum. Normally, in healthy elderly people, dopamine levels are sufficiently high to counter the natural effects of acetylcholine in the caudate and putamen. In people with Parkinson's disease, however, the reduction in striatal dopamine leads to an imbalance, with a relative excess of acetylcholine affecting motor control. Acetylcholine antagonists such as Artane provide some relief for a limited range of movement disorders, in particular tremor, although they are associated with side effects such as visual disturbance, confusion and hallucinations in elderly people, urinary retention and a dry mouth. They are usually prescribed in combination with levodopa to obtain maximum benefit. (4) Adamantane derivatives (glutamate blockers)

Adamantane derivatives such as Amantadine are sometimes used as a first line of defence in the treatment of movement disorders in Parkinson's disease. Although they can initially have beneficial effects in the newly diagnosed, levodopa preparations are soon added when movement disorders become more troublesome. In addition to augmenting the presynaptic

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End of dose dyskinesia

Peak dose dyskinesia

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Biphasic dyskinesia

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'I, I'",

100

C

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~Q) Go

60

120

180

240

300

360

Time (minutes) "On!off" phenomenon

---- ------- Biphasic dyskinesia

Peak dose dyskinesia

- - - - - -

End of dose dyskinesia

figure 2. Common motor fluctuations observed in end-stage Parkinson's disease.

synthesis and release of dopamine (Reynolds 1996), it appears that drugs such as Amantadine block overactivity of glutamate in the pathways from the striatum to the subthalamic nucleus and substantia nigra. Excessive levels of glutamate may act as a neurotoxin. Moreover, there is limited evidence that adamantane derivatives may have a neuroprotective effect, possibly by acting as anti-oxidants in the substantia nigra of the brainstem or via their antiglutamate effects (Reynolds 1996). (5) Neuroprotective agents

Monoamine oxidase B (MAO B) inhibitors, such as selegiline (Eldepryl) block the catabolism of dopamine by microglia and astrocytes in the basal ganglia (Youdim and Riederer 1997). As a result, the availability of dopamine at post-synaptic receptor sites is increased. This means that patients can sometimes be given lower doses of levodopa when selegeline is added to the medication regimen. These drugs may also have a neuroprotective effect, by reducing free radical formation and oxidation of substantia nigra neurones, although the recent "DATATOP" and UKPDRG drug trials failed to confirm this hypothesis (Lees 1995). In fact Lees (1995) found that selegiline in

combination with levodopa was associated with an increase in mortality after three years of use.

Motor fluctuations Despite the beneficial effects that levodopa, dopamine agonists and the adamantane derivatives can initially have on motor performance in Parkinson's disease, the benefits are shortlived (Barbeau 1974, Fahn 1974, Marsden and Parkes 1976). After a period of approximately five years, motor fluctuations develop in at least 50 per cent of patients (Mouradian and Chase 1994) and increase in severity as the disease progresses. Initially the motor fluctuations present as a wearing off effect which occurs at the end of the medication dose. The person experiences a shift from near normal mobility (known as the "on" phase) to a state of immobility (known as the "off" phase - Figure 2). Later, as the disease progresses, abnormal involuntary extra movements (dyskinesias) can become evident. Most often these manifest as peak dose dyskinesias which are generally choreiform. Bi-phasic and end of dose dyskinesias are also reasonably common and can be choreiform or

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Determine the purpose of measurement

1 Select appropriate level of measurement Disability

Motor Performance (tasks)

Movement Disorders

~

1

.~

Independence Function Well being Activity level Life satisfaction

Walking Turning Standing up Sitting down Rolling over Prehension Manipulation

Hypokinesia Akinesia Dyskinesia Tremor Rigidity Postural instability

~

I

T

/

I

Measure patient both "on" and "off" medication

t

Repeat tests over time to clarify effects of medication, physiotherapy and natural progression of the disease

Figure 3. Clinical decision making process used by physiotherapists to quantify motor fluctuations in Parkinson's disease.

dystonic in type (Luquin et alI992, Muenter et al 1977 - Figure 2). Painful off-phase dystonias, often at night, can also occur in some people. Patients typically describe these as feeling like muscular cramps, low back pain or clawing of the toes. With long term use of dopamimetics over periods of 10-30 years, different combinations of these motor fluctuations inevitably develop in the majority of people and, in some cases, can be just as disabling as the disease itself. Dyskinesias are thought to be mediated by D2 receptors on the striatal projections to the indirect pathway. However, the reason why peak dose dyskinesias and the on-off phenomenon eventually occur after prolonged use of Parkinson's disease

medication is not completely clear. Possible explanations include that (i) drug induced changes in the striatum alter the sensitivity ofDI and D2 receptors; (ii) pulsatile delivery and absorption of levodopa with oral doses leads to fluctuations in blood and brain concentrations of this drug (iii) there is a heightened sensitivity of the dopamine receptors in the striatum which appears to be due to functional denervation associated with prolonged depletion of dopamine ancovic and Marsden 1988). For a more detailed review of these issues, readers are referred to Fabbrini et al (1988), Marsden and Parkes (1986) and Nutt et al (1992). In evaluating motor fluctuations in Parkinson's disease, two components

cr

to the response to levodopa and apomorphine need to be considered. There is a short duration response, which occurs over a period of hours, and a long duration response which occurs over days and is presumably related to the cumulative effect of multiple doses. In de novo patients (drug naive with a short history of motor symptoms) the short duration response is present in some but not all cases (Gancher et al 1988) and the long duration response is present by 15 days of treatment (Quattrone et alI995). However, these responses can be difficult to detect clinically at the onset of drug treatment, as they usually occur subtly in people with an apparently stable response. As the disease progresses and the duration of drug treatment increases, the short duration responses to levodopa and apomorphine decrease. This means that the short duration effects of levodopa and apomorphine do not last as long, even though the size of the response (the difference between baseline performance and peak motor performance) remains constant as the disease progresses and fluctuations develop. Therefore the scheduling of drug administration might need to be altered, for example by changing administration from 6-hourly to 4hourly. The long duration response is much less studied and understood. It is generally measured as the deterioration in baseline motor performance after total drug withdrawal and represents at least one third of the total response to regular levodopa. The degree to which the long duration response changes with disease longevity and the duration of drug treatment is currently under investigation. The clinical implications of these findings for physiotherapists are that: (i) motor performance can vary according to when the person is observed in relation to the timing of medication and (ii) true baseline performance off drugs may not be reached for 1-2 weeks.

Measuring motor fluctuations In addition to movement rehabilitation in Parkinson's disease, the role of the physiotherapist is to measure any motor fluctuations that occur

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according to the dosage, scheduling and type of medication prescribed. This role can include: • measuring the person's response capacity to drugs by conducting dose response trials (test doses) and plotting dose response curves for the short duration response; • determining the relative contributions of involuntary movements and hypokinesia/ akinesia to motor disability; • monitoring the person's motor response to medication during the course of physiotherapy and differentiating changes in motor performance resulting from physiotherapy and drugs; and • advising the health care team of the person's motor response to medications prescribed by the neurologist. Parkinson's disease is prevalent amongst elderly people and, with the rapid increase in the proportion of elderly people within the Australian population, the demand for physiotherapy assessment and treatment of movement disorders in Parkinson's disease has sharply increased. It is now commonplace for medical practitioners to refer patients to a physiotherapist for objective assessment of the person's motor response to medication, hence the ability to do this needs to be recognised as a basic competency. Most often the request from the neurologist is for a dose response trial (DRT) to evaluate the short duration response to a particular medication. In the Clinical Notes section of this edition of the Australian Journal of Physiotherapy, a step-by-step guide on how to perform a D RT is presented, illustrated by a case example. The remainder of this paper will focus on the process and tools that can be used by physiotherapists to monitor changes in motor performance that occur with Parkinson's disease medication. In charting the person's motor response to medication, the physiotherapist can monitor at the level of disability, motor function or movement disorders. A range of

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disability scales are available that enable the clinician to quickly screen for gross motor status. Perhaps the best known of these is the Hoehn and Yahr (1967) scale, which provides a brief snapshot of the person's mobility and independence. The drawback of this scale is that it lacks sensitivity and is able to discriminate only dramatic changes in disability status. Therefore most clinicians also use either the Modified Webster scale (Kempster et aI1989), the Unified Parkinson's Disease Rating scale (UPDRS) (Fahn et aI1987), the North West University Disability scale (Canter 1961) or the Columbia scale (Yahr et a11969) to quickly screen for level of disability. Although the Functional Independence Measure (FIM) (Granger et a11986) has been shown to be a useful measure of disability in stroke patients and frail elderly people, it has not yet been validated in individuals with Parkinson's disease. Alternatively, the Human Activity Profile (Fix and Daughton 1988) can provide the clinician with a comprehensive summary of the person's motor activity which provides an indirect indication of disability status. In the clinical setting, physiotherapists most often measure change in motor peiformance by testing patients on several functional tasks such as walking, turning, standing up, sitting down, rolling over in bed, reaching, grasping, manipulating objects and writing (Table 3). The usual procedure is to time performance for a selection of these actions using a stopwatch and to observe for deviations in the person's movement kinematics. For analysing walking, the physiotherapist can also use a computerised stride analyser (CSA)t to quantify temporal and spatial parameters of gait, such as the velocity of walking, stride length, cadence and the duration of single limb support phases. Although high retest reliability has been established for CSA measures for patients in the "on" stage of the medication cycle (Morris et al 1996a and 1996b), the validity of visual observations and stopwatch measures for movement analysis in Parkinson's disease remains to be established.

A further role of the physiotherapist is to quantify the severity of movement disorders in Parkinson's disease and to examine the degree to which movement disorders affect motor performance and functional ability. Whereas measures of gait hypokinesia and postural instablity have been examined for retest reliability, discriminant validity and predictive validity (Morris et al 1996a, Schenkman 1997, Smithson et al 1998), tests of akinesia, rigidity, tremor and dyskinesia require further validation (Kennard et aI1984). Some clinicians rely on qualitative measures including visual observation, palpation and passive and active movement testing to make decisions about the severity of movement disorders and their response to Parkinson's disease medication. Qualitative measures of this type simply provide a clinical impression and do not yield data on the severity of specific movement disorders or their impact on task performance. The combination of tests used to quantify motor status will vary from individual to individual, according to the person's problems and the aims of the measurement process. If, for example, the aim is to quantify whether postural instability changes according to levodopa status, the physiotherapist might choose to use the Pastor test (Pastor et al 1996) combined with tests of steady standing and the Functional Reach test (see Table 3) at peak dose and again at the end of dose. On the other hand, if the primary aim is to chart upper limb status, the clinician would typically observe for tremor, hypokinesia and dyskinesia; test the person on the Purdue Pegboard (Tiffin 1979); obtain a handwriting sample; and observe the person performing functional upper limb tasks such as picking up the dosette box from the bedside table and removing the medication. As well as determining an appropriate level of analysis (disability, motor function or movement disorders), the physiotherapist needs to carefully consider the timing of measurement. To be able to detect change in

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performance, it is important to first have baseline measures of stability against which future performance can be compared. In Parkinson's disease, two baselines need to be charted: (i) an on-phase baseline, representing the person's typical performance at peak dose in the medication cycle; and (ii) an off-phase baseline, representing the person's typical performance at the end of the dose, when blood concentrations of medication are low. For people on a 4-hourly medication regimen it is customary for the on-phase measurements to be obtained one hour after the Parkinson's disease medication and the off-phase measures to be obtained half an hour prior to the next dose. Due to the typical fluctuations in performance, usually three trials of a given test are needed to establish a reliable baseline sample, such as three 10m walking trials, three handwriting samples or three trials on the Purdue Pegboard test. It is useful to document the assessment findings using colour coded assessment forms, for example a green assessment form for on-phase readings and a pink form for the off-phase readings (Morris and Iansek 1997). Fluctuations in motor performance can be measured: (i) within a single Parkinson's disease medication cycle, typically 4-6 hours duration; (ii) across a 12 or 24 hour period; (iii) across five days (one working week) of an inpatient stay; (iv) across longer periods ranging from weeks to months. When testing within a single cycle, frequent sampling of motor performance using a small battery of tests is required. For example, at the Kingston Centre in Melbourne, the response to standard levodopa is often charted by testing the person every 15 minutes using the 10m walk, TimedUp-And-Go test and Purdue Pegboard test. The first trial commences half an hour before the medication is taken, and then subsequent trials occur every 15 minutes for the duration of that cycle (frequently 4 hours). If the aim is to evaluate motor fluctuations throughout the course ofa day, less frequent sampling is needed, and the physiotherapist can use more lengthy testing procedures if required. The

person could, for example, be measured every two hours commencing at 8 am using the CSA, a battery of postural stability tests (Smithson et al 1998), the Purdue Pegboard test and a dyskinesia rating scale such as in the UPDRS (Fahn et al 1987). When charting motor fluctuations across periods ranging from one week to a number ofyears, it is customary for measures to be obtained on each occasion in relation to the on and off-phases of the mid-morning dose of medication (which is often taken at 10 am). As discussed previously, the selection of which clinical tests to include in the battery for that person will depend on the major movement disorders that limit functional performance. The clinical decision making process used by physiotherapists to determine the appropriate level of measurement is detailed in Figure 3. The figure highlights the need to repeat tests over time in order to chart the patient's progress. There may be a further need to differentiate the effects of medication from physiotherapy and the natural progression of the disease. This is complex and can be tackled in a variety of ways. As a guide, it should be kept in mind that changes associated with medication are often large in magnitude, occur rapidly within the first hour after it is administered, have a short duration response of approximately 4-6 hours and a much smaller long duration response for up to 15 days. A DRT is the best way to measure the short duration response of medication; the long duration response can be determined only by a "drug holiday" which is seldom considered necessary. To differentiate the shortterm effects of physiotherapy from medication, motor performance is first tested at peak dose of the medication cycle then training immediately occurs. Training for a motor function such as walking or standing up may take 20-40 minutes and is followed by prompt remeasurement before the off-phase occurs. This procedure reveals the contribution of physiotherapy over and above the effects of medication. Alternatively, the short-term effects of physiotherapy can be assessed by

measuring motor performance before and after a training session prior to the person's first morning dose of antiparkinsonian medication. Although this more clearly differentiates the effects of physiotherapy and medication, patient compliance may be low, as testing needs to occur before the first dose (usually at 6 am or 8 am) and before breakfast is consumed. This procedure is therefore most suitable for inpatients rather than patients resident in the community. To ascertain the natural progression of the disease, patients are usually tested at 3monthly intervals under optimal conditions (at peak dose of the 10 am medication after physiotherapy training) as well as in the off phase of the lOam dose without physiotherapy (when physiotherapy and medication are less likely to obscure effects due to disease progression). Alternatively they can be tested at 3-monthly intervals prior to the first morning dose of medication. In summary, there is an increasing need for physiotherapists to quantify changes in motor performance that occur with Parkinson's disease medication and to communicate findings to neurologists and other health professionals. In order to do this competently, there is a need to have up to date knowledge of the pathophysiology of Parkinson's disease, the mode of action of the range of medications available as well as skills in objectively measuring motor fluctuations. By carefully documenting changes in performance over time, the most effective treatment program can be implemented by the interprofessional team. t Clinical Stride Analyser: A computerised footswitch system that enables measurement of the temporal and spatial parameters of gait.

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ORIGINAl ARTIClE

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