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Parkinson’s Diseases
Version 1 Final
EBM – Parkinson’s Diseases
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Introduction
“Parkinson’s disease is characterised by impairment of movement, muscle rigidity,
and tremor. It was named after an accomplished English doctor called James
Parkinson (1755-1824) who after patiently observing and carefully listening to six
sufferers with involuntary shaking of the body, differentiated it from other known
medical causes at that time. At first he called it the shaking palsy, which later
became known as Parkinson’s disease. A further distinction is made between true
Idiopathic Parkinson’s disease when the cause of the disease is unknown, and
diseases with similarities to Parkinson’s such as hypothyroidism and degenerative
diseases of the nervous system, which are often referred to as Parkinsonism.” [1]
Description
Idiopathic Parkinson’s disease (PD) is a progressive neurodegenerative condition
resulting from the selective loss of the dopamine-containing neurons of the
substantia nigra. The diagnosis is primarily clinical based on history and
examination, although Parkinson’s disease can be distinguished from other causes
of Parkinsonism as it is usually asymmetrical and responsive to dopaminergic
treatment. There is no consistently reliable test that can distinguish PD from other
conditions and a definitive diagnosis can only be obtained at post mortem.
Parkinsonism describes a syndrome of tremor, rigidity and bradykinesia of which
idiopathic Parkinson’s disease is the main cause but there are also many other
causes. These include drugs (7%), multiple cerebral infarction and degenerative
conditions such as progressive supra-nuclear palsy (PSP) and multiple system
atrophy (MSA).
Prevalence
Parkinson’s Disease is estimated to affect 100–180 people per 100,000 of the
population (between 6 and 11 people per 6000 of the general population in the UK)
and has an annual incidence of 4–20 per 100,000. It is among the commonest
causes of neurological disability in the United Kingdom.
Parkinson's disease affects about 1% of people ≥ 60 years and 0.4% of those > 40
years. The mean age at onset used to be in the late 50s but is now thought to be in
the early to mid 60s. Rarely, Parkinson's disease begins in childhood or
adolescence (juvenile parkinsonism).
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Aetiology
The aetiology of Parkinson's disease is unknown, however, a number of factors
have been implicated: [3]
The toxin MPTP causes a clinical syndrome identical to Parkinson's Disease. MPTP
is converted into its active form MPP+ by monamine oxidase type B. This is taken
up by the Dopamine transport systems of dopaminergic cells to cause disruption in
the mitochondrial respiratory chain affecting mitochondrial complex 1 activity.
Similarly impaired mitochondrial function is seen in normal Parkinson's disease
suggesting that there may be a free radical insult that causes the disease.
Conversely, some environmental agents appear to reduce the risk of Parkinson’s
disease, such as caffeine and some chemicals in cigarette smoke.
Genetic factors
About 15 % of patients have a first degree relative with Parkinson’s disease, without
any clear mode of inheritance. Genetic factors are thought to be of little importance
in Parkinson's Disease as a result of twin studies, however, mitochondrial
inheritance has to be considered and different expression of the disease in twins
with later onset of the disease excluded in the first studies has meant that some
authorities still believe that genetic influences are important.
Ageing
Dopaminergic neurones are affected by the ageing process declining at a rate of
about 5% per decade. This rate of ageing would not account for Parkinson's disease
alone but when combined with an environmental insult may explain its late age
distribution.
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Diagnosis
Diagnosis is clinical. Clinical criteria have been described by Gelb et al. [Appendix 1]
Presenting Features
The three key features are tremor, rigidity and bradykinesia. In most patients, the
disease begins insidiously with a resting tremor (pill-rolling tremor) of one hand. The
tremor is slow and coarse and maximal at rest. It lessens during movement, and is
absent during sleep. It is enhanced by emotional tension or fatigue.
Usually, the hands, arms, and legs are most affected, in that order. The jaw, tongue,
forehead, and eyelids may also be affected, but not the voice. Tremor may become
less prominent as the disease progresses.
Rigidity is the raised resistance noted during passive joint movement, and can
develop a cogwheel character when the limb is tremulous. As rigidity progresses,
movement becomes slow (bradykinesia), decreased (hypokinesia), and difficult to
initiate (akinesia). Bradykinesia can be the most disabling feature of PD, and may
cause problems with fine motor tasks. Rigidity and hypokinesia may contribute to
muscular aches and sensations of fatigue. Patients can also have postural
instability, usually in later disease, which may increase their risk of falls. The
characteristic gait is of reduced arm swing and slow, shuffling movements.
The face becomes mask like, with mouth open and reduced blinking.
Early on, patients may appear depressed because facial expression is lacking and
movements are decreased and slowed. Speech becomes hypophonic, with
characteristic monotonous, stuttering dysarthria. Hypokinesia and impaired control
of distal musculature cause micrographia (writing in very small letters) and make
activities of daily living increasingly difficult. [4]
Key Findings on Examination
Parkinson's disease is suspected in patients with characteristic resting tremors,
decreased movement, or rigidity.
When a clinician moves a rigid joint, sudden, rhythmic jerks due to variations in the
intensity of the rigidity occur, producing a ratchet-like effect (cogwheel rigidity).
Other characteristic signs (e.g. infrequent blinking, lack of facial expression,
impaired postural reflexes, characteristic gait abnormalities i.e. festinant gait) help to
confirm the diagnosis. Sufferers sometimes have difficulty initiating movement and
then, when in motion, are prone to hurry with their upper body hunched forwards.
When they try to stop they are sometimes unable to do so and hence festination
continues.
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Differential Diagnoses
The differential diagnosis of PD includes normal ageing, drug induced parkinsonism,
essential tremor, multiple cerebral infarcts, Parkinson’s plus syndromes, vascular
parkinsonism, Lewy body dementia and hydrocephalus. History should include
questions about head trauma, stroke, hydrocephalus, exposure to drugs and toxins,
and symptoms or history of other degenerative neurological disorders. [5]
Essential tremor
A common usually hereditary or familial disorder of movement that is characterized
by uncontrolled trembling of the hands and often involuntary nodding of the head
and tremulousness of the voice that is exacerbated by anxiety and by activity.
Drug induced parkinsonism:
Any drug that blocks the action of dopamine is likely to cause Parkinsonism. Drugs
used to treat schizophrenia and other psychotic disorders such as behaviour
disturbances in people with dementia, (known as neuroleptic drugs) are probably the
major cause of drug induced Parkinsonism worldwide.
As well as neuroleptics some other drugs can cause drug induced Parkinsonism.
These include prochlorperazine (stemetil) and metoclopramide (Maxolon) used to
treat dizziness, nausea and vomiting. It is considered that these are two of the most
common causes of drug induced Parkinsonism in the elderly - something which is
not always recognised.
Multiple cerebral infarcts
Multiple infarcts in the basal ganglia and subcortical white matter may present with
gait abnormalities. Tremor is not often a feature. A CT or MRI scan will demonstrate
extensive small vessel disease.
Hydrocephalus
An abnormal increase in the amount of cerebrospinal fluid within the cranial cavity
that is accompanied by expansion of the cerebral ventricles, enlargement of the skull
and especially the forehead, and atrophy of the brain.
Lewy Body Dementia
Presents with progressive Parkinsonism and early dementia. It is associated with
hallucinations, behavioural disturbance and psychosis.
Trauma - 'punch drunk' syndrome
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Other neurodegenerative diseases:
progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome).
An uncommon neurological disorder that is of unknown aetiology, that typically
occurs from late middle age onward, and that is marked by loss of voluntary
vertical eye movement, muscular rigidity and dystonia of the neck and trunk,
pseudobulbar paralysis, bradykinesia, and dementia.
multiple system atrophy.
Wilson's disease
A hereditary disease that is characterized by the accumulation of copper in the body
(as in the liver, brain, or cornea) due to abnormal copper metabolism associated
with ceruloplasmin deficiency, that is determined by an autosomal recessive gene,
and that is marked especially by liver dysfunction and disease and neurologic or
psychiatric symptoms.
Post encephalitic parkinsonism
encephalitis lethargica (epidemic viral encephalitis in which somnolence is marked).
Toxins:
carbon monoxide
manganese
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Treatment
Pharmacological
Motor Symptoms
Treatment should be started when symptoms start to cause disability. There is no
single drug of choice in the initial pharmacotherapy of early PD, although definitive
treatment of early PD is with levodopa or a dopamine agonist. Dopamine agonists
are a good choice in early PD and in treatment of younger patients. They are less
effective than L-dopa but will control symptoms for a few years thus delaying the
need for L-dopa. In the elderly, L-dopa is the first line choice as it is better tolerated.
L-dopa’s main problem is that patients tend to develop motor fluctuations with ‘on
off’ effects and also develop dyskinesias. Table 1 may help to guide the reader
through the following section. [2]
Table 1 Options for initial pharmacotherapy in early PD
Initial therapy
First-choice
Symptom
Risk of side effects
for early PD
option
control
Motor
Other
complications
adverse
events
Levodopa
+++
Dopamine
++
agonists
MAO-B inhibitors
+
Anticholinergics
Lack of
Lack of
Lack of
evidence
evidence
evidence
Beta-blockers
Lack of
Lack of
Lack of
evidence
evidence
evidence
Amantadine
Lack of
Lack of
Lack of
evidence
evidence
evidence
KEY
+++ = Good degree of symptom control
++ = Moderate degree of symptom control
+ = Limited degree of symptom control
= Evidence of increased motor complications/other adverse events
= Evidence of reduced motor complications/other adverse events
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Levodopa
Levodopa may be used as a symptomatic treatment for people with early PD.
The dose of levodopa should be kept as low as possible to maintain good function in
order to reduce the development of motor complications.
Dopamine agonists
Dopamine agonists may be used as a symptomatic treatment for people with early
PD. Non ergot agonists should be used.
A dopamine agonist should be titrated to a clinically efficacious dose. If side effects
prevent this, another agonist or a drug from another class should be used in its
place.
Monoamine oxidase B inhibitors
MAO-B inhibitors may be used as a symptomatic treatment for people with early PD.
Beta – blockers
Beta – blockers (Beta-adrenergic antagonists) may be used in the symptomatic
treatment of selected people with postural tremor in PD, but should not be drugs of
first choice. These are not generally used at all nowadays.
Amantadine
Amantadine may be used as a treatment for people with early PD but should not be
a drug of first choice.
Anticholinergics
Anticholinergics may be used as a symptomatic treatment typically in young people
with early PD and severe tremor, but should not be drugs of first choice due to
limited efficacy and the propensity to cause neuropsychiatric side effects.
Most people with PD will develop, with time, motor complications and will eventually
require levodopa therapy. Adjuvant drugs to take alongside levodopa have been
developed with the aim of reducing these motor complications and improving quality
of life.
There is no single drug of choice in the pharmacotherapy of later PD. Table 2 may
help to guide the reader through the following section.
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Table 2 Options for adjuvant pharmacotherapy in later PD
Adjuvant
First-
Symptom
Risk of side effects
therapy for later
choice
control
PD
option
Motor
Other adverse
complications
events
Dopamine
++
agonists
COMT inhibitors
++
MAO-B inhibitors
++
Amantadine
NS
Apomorphine
+
KEY
+++ = Good degree of symptom control
++ = Moderate degree of symptom control
+ = Limited degree of symptom control
= Evidence of increased motor complications/other adverse events
= Evidence of reduced motor complications/other adverse events
NS = Non-significant result
Dopamine agonists
Dopamine agonists may be used to reduce motor fluctuations in people with later
PD.
A dopamine agonist should be titrated to a clinically efficacious dose. If side effects
prevent this, then another agonist or a drug from another class should be used in its
place.
Catechol-O-methyl transferase inhibitors(Entacapone, Tolcapone)
Catechol-O-methyl transferase (COMT) inhibitors work by lengthening the half life of
circulating L-dopa thus helping prevent the phenomenon of end of dose ‘wearing
off’. It is used to reduce motor fluctuations in people with later PD.
People with later PD may require the addition of entacapone and triple combination
preparations of levodopa, carbidopa and entacapone are available in a range of
dosages to facilitate this.
Tolcapone should only be used after entacapone has failed in people with later PD
due to lack of efficacy or side effects.
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Monoamine oxidase B inhibitors
MAO-B inhibitors may be used to reduce motor fluctuations in people with later PD.
Amantadine
Amantadine may be used to reduce dyskinesia in people with later PD.
Apomorphine
Intermittent apomorphine injections may be used to reduce “off” time in people with
PD with severe motor complications.
Continuous subcutaneous infusions of apomorphine may be used to reduce “off”
time and dyskinesia in people with PD with severe motor complications.
Non Motor Symptoms
As a result of autonomic dysfunction, patients on anti-parkinsonian drugs can have
problems with constipation, urinary symptoms and postural hypotension. To aid
constipation they should consume a high-fiber diet. Dietary supplements (e.g.
psyllium) and stimulant laxatives (e.g. bisacodyl 10 to 20 mg orally once/day) can
help.
Clinicians should be aware of dopamine dysregulation syndrome, an uncommon
disorder in which dopaminergic medication misuse is associated with abnormal
behaviours, including hypersexuality, pathological gambling and stereotypic motor
acts. This syndrome may be difficult to manage.
Physical
Maximizing activity is a goal. Patients should perform daily activities to the maximum
extent possible. If they cannot, a regular exercise program or physical therapy may
help condition them physically and teach them adaptive strategies. To this end the
National Institute for Health and Clinical Evidence (NICE) [2] has identified a number
of key priorities including:
Physiotherapy
Physiotherapy should be available for people with PD. Particular consideration
should be given to:
gait re-education, improvement of balance and flexibility
enhancement of aerobic capacity
improvement of movement initiation
improvement of functional independence, including mobility and
activities of daily living
provision of advice regarding safety in the home environment
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Coping with postural hypotension may be aided by avoiding rapid
changes of posture, large meals, excessive alcohol, warm temperatures
and excessive straining.
Occupational Therapy
Occupational therapy should be available with the particular intention of:
maintenance of work and family rôles, employment, home care and
leisure activities
improvement and maintenance of transfers and mobility
improvement of personal self-care activities, such as eating, drinking,
washing and dressing
environmental issues to improve safety and motor function
cognitive assessment and appropriate intervention.
Speech and Language Therapy
Speech and language therapy should be available for:
improvement of vocal loudness and pitch range, including speech
therapy programmes
teaching strategies to optimise speech intelligibility
ensuring an effective means of communication is maintained throughout
the course of the disease, including use of assistive technologies
review and management to support the safety and efficiency of
swallowing and to minimise the risk of aspiration.
The Parkinson's Disease Society
www.parkinsons.org.uk is the leading charity
dedicated to supporting all people with PD, their families, friends and carers.
Surgical
Currently three surgical options are available for PD.
These are SubThalamic Nucleus stimulation (STN), Globus Pallidus interna
stimulation (GPi) and Thalamic stimulation.
STN and GPi have to date shown no difference in efficacy or safety and the
indications for either are the same:
have motor complications that are refractory to best medical treatment,
are biologically fit with no clinically significant active comorbidity,
are levodopa responsive
have no clinically significant active mental health problems, for example,
depression or dementia.
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Bilateral stimulation of the subthalamic nucleus is associated with significant
improvement in motor function and reduction of antiparkinsonian medications in the
first 12 months after surgery. [6]
GPi is rarely performed in the United Kingdom at present though it is sometimes
undertaken when STN is not possible.
Thalamic deep brain stimulation may be considered as an option in people with PD
who predominantly have severe disabling tremor and where STN stimulation cannot
be performed. [2]
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Prognosis
Parkinson's disease is a progressive disorder which starts with mild unilateral
involvement and progresses to complete dependency. It is usually staged in five
stages; [3]
Stage I Unilateral involvement only
Stage II Bilateral involvement without impairment of balance
Stage III Impairment of balance and functional restriction
Stage IV Fully-developed disease retaining ability to walk and stand
unassisted but otherwise markedly incapacitated
Stage V Bed-bound or wheelchair bound unless aided
Untreated, the disorder progresses to total disability, often accompanied by general
deterioration of all brain functions, and may lead to an early death.
Treated, the disorder impairs people in varying ways. Most people respond to some
extent to medications. The extent of symptom relief, and how long this control of
symptoms lasts, is highly variable. The side effects of medications may be severe.
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Main Disabling Effects
Patients have difficulty starting to walk, turning, and stopping. The posture becomes
stooped.
The gait becomes shuffling with short steps, and the arms are held flexed to the
waist and do not swing with the stride.
There is a tendency to fall forward (propulsion) or backward (retropulsion) known as
postural instability. This relates to loss of the involuntary movements people
automatically make to maintain their balance when standing. Impairment of postural
reflexes causes poor balance and may increase the risk of falls.
Dementia and depression are common. Dementia develops in about 40% of
patients, and depression may affect nearly half of all patients. Depression is
associated with lower cognition, history of depression, and a higher Parkinson's
Disease Rating Scale score. [7] [Appendix 2]
PD patients with major depression have a significantly faster decline in activities of
daily living and cognitive functions, and a faster progression along the stages of the
illness as compared to non-depressed PD patients. Depression should be treated
with SSRIs as tricyclics may exacerbate postural hypotension. There are very few
useful drug trials of antidepressant use in PD.
Some patients do experience hallucinations, usually visual. These can be a feature
of Lewy body dementia but also a side effect of dopamine agonist therapy. However
the Parkinson’s Disease Society reports that most people do not find them
threatening or distressing and are aware that the images or sounds are not real and
are able to cope with them.
Patients may have orthostatic hypotension, constipation, or urinary hesitancy. Some
patients have difficulty swallowing and are at risk of aspiration.
Patients cannot perform rapidly alternating movements.
Sensation and strength are usually normal. Reflexes are normal but may be difficult
to elicit because of marked tremor or rigidity.
Seborrheic dermatitis is common.
Parkinson’s disease rating scale (PDRS) of Webster et al. [9] [Appendix 2] is the
most widely used for the evaluation of clinical impairment in PD. A simpler test for
the impact on activities of daily living using 5 items (Handipark) was proposed in
2003 but has not yet been verified for general use. [10]
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Appendix A - Clinical Criteria of Gelb et al for the
Diagnosis of Idiopathic Parkinson’s Disease
Gelb et al used clinical features to identify patients with idiopathic Parkinson's disease. These
can help accurately classify symptomatic patients. The authors are from the University of
Michigan and the National Institute of Neurological Disorders and Stroke.
Clinical features of Parkinson's disease:
(1) resting tremor
(2) rigidity
(3) asymmetric onset
(4) bradykinesia
Features suggesting an alternative diagnosis:
(1) dementia preceding motor symptoms
(2) dementia in first year after symptom onset
(3) prominent postural instability in the first 3 years after symptom onset
(4) freezing phenomenon in the first 3 years after symptom onset
(5) supranuclear gaze palsy (other than restriction of upward gaze)
(6) slowing of vertical saccades (rapid small movements in both eyes that occur when
changing the point of fixation)
(7) severe, symptomatic dysautonomia unrelated to medications
(8) presence of located focal brain lesion that can produce parkinsonian symptoms
(9) drug capable of causing Parkinson's disease taken within the past 6 months
Criteria for definite Parkinson's disease - both of the following:
(1) meets criteria for possible Parkinson's disease (below)
(2) histologic evidence of Parkinson's disease found on brain examination at autopsy
Criteria for probable Parkinson's disease - all 3 of the following:
(1) 3 or all 4 of the clinical features of Parkinson's disease
(2) no features present indicating an alternative diagnosis (items #3 and #4 require
symptoms for at least 3 years)
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(3) substantial and sustained response to levodopa or dopamine agonist
Criteria for possible Parkinson's disease - all 3 of the following:
(1) 2 or more of the 4 clinical features of Parkinson's disease
(2) either no features for an alternative diagnosis are present after 3 years OR none of the
features are present to date if disease duration is less than 3 years
(3) either the patient has a substantial and sustained response to levodopa or a dopamine
agonist OR the patient has not had an adequate clinical trial (viz, NOT adequate clinical
trial of medication with no or inadequate or nonsustained response).
References:
Gelb DJ, Oliver E, Gilman S. Diagnostic criteria for Parkinson's disease. Arch Neurology.
1999; 56: 33-39.
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Appendix B - The Parkinson’s Disease Rating Scale
(PDRS) of Webster et al
Webster developed a rating scale for patients with Parkinsons disease based on 10 clinical
findings. The scale indicates the severity of disease and the clinical impairment. Changes in
the scale over time can reflect changes due to disease progression or therapeutic
interventions. The author is from the University of Minnesota.
Parameters:
(1) bradykinesia of hands (including handwriting)
(2) rigidity
(3) posture
(4) upper extremity swing
(5) gait
(6) tremor
(7) facies
(8) seborrhea
(9) speech
(10) self-care
Parameter
Finding
Points
bradykinesia of hands
no involvement
0
detectable slowing of the supination- 1
pronation rate; beginning difficulty in handling
tools, buttoning clothes, and with handwriting
moderate slowing of the supination- 2
pronation rate in one or both sides; moderate
impairment of hand function; handwriting is
greatly impaired, micrographia present
severe slowing of the supination-pronation 3
rate; unable to write or button clothes;
marked difficulty in handling utensils
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rigidity
non-detectable 0
detectable rigidity in neck and shoulders; 1
activation phenomenon is present; one or
both arms show mild, negative, resting
rigidity
moderate rigidity in neck and shoulders; 2
resting rigidity is present if patient is not on
medications
severe rigidity in neck and shoulders; resting 3
rigidity cannot be reversed by medication
posture
normal posture; head flexed forward less 0
than 4 inches
beginning poker spine; head flexed forward 1
more than 5 inches
beginning arm flexion; head flexed forward 2
up to 6 inches; one or both arms raised but
still below waist
onset of simian posture; head flexed forward 3
more than 6 inches; one or both hands
elevated above the waist; sharp flexion of
hands, beginning interphalangeal extension;
beginning flexion of knees
upper extremity swing
swings both arms well
0
one arm definitely decreased in amount of 1
swing
one arm fails to swing
2
both arms fail to swing
3
gait
steps out well with 18-30 inch stride; turns 0
about effortlessly
gait shortened to 12-18 inch stride; 1
beginning to strike one heel; turn around time
slowing; requires several steps
stride moderately shortened to 6-12 inches; 2
both heels beginning to strike floor forcefully
onset of shuffling gait; steps less than 3 3
inches; occasional stuttering-type or blocking
gait; walks on toes; turns around very slowly
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tremor
no detectable tremor found
0
less than 1 inch of peak-to-peak tremor 1
movement observed in limbs or head at rest,
or in either hand while walking or during the
finger-to-nose testing
maximum tremor envelope fails to exceed 4 2
inches; tremor is severe but not constant and
patient retains some control of hands
tremor envelope exceeds 4 inches; tremor is 3
constant and severe; patient cannot get free
of tremor while awake unless it is a pure
cerebellar type; writing and feeding self are
impossible
facies
normal; full animation; no stare
0
detectable immobility; mouth remains 1
closed; beginning features of anxiety or
depression
moderate immobility; emotion breaks 2
through at markedly increased threshold; lips
parted some of the time; moderate
appearance of anxiety or depression;
drooling may be present
frozen facies; mouth opens >= 0.25 inches; 3
drooling may be severe
seborrhea
none 0
increased perspiration, secretions remain thin 1
obvious oiliness present and secretion much 2
thicker
marked seborrhea; entire face and head 3
covered by thick secretion
speech
clear, loud, resonant, easily understood
0
beginning of hoarseness, with loss of 1
inflection and resonance; good volume and
still easily understood
moderate hoarseness and weakness; 2
constant monotone, unvaried pitch; beginning
of dysarthria, hesitance, stuttering, difficult to
understand.
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marked harshness and weakness; very 3
difficult to hear and to understand
self-care
no impairment
0
still provides full self-care, but rate of 1
dressing definitely impeded; able to live alone
and may be employable
requires help in certain critical areas; very 2
slow in performing most activities but
manages by taking much time
continuously disabled; unable to dress, feed 3
self or walk alone
Parkinsons disease rating scale =
= SUM(points for all 10 parameters)
Interpretation:
• minimum score: 0
• maximum score: 30
• The higher the score the greater the disease severity and disability.
Scale Disability
1 − 10
early illness
11 - 20
moderate
21 − 30
severe or advanced
References:
Webster DD. Critical analysis of the disability in Parkinsons disease. Modern Treatment.
1968 (March); 257-282. (pages 279-281
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References
[1] Butlin, J Parkinson’s Disease Positive Health web site
(http://www.positivehealth.com/permit/Articles/Neurological/butln53.htm)
[2] National Institute for Health and Clinical Excellence
Parkinson’s Disease Clinical Guidelines 35 June 2006
[3] Liverpool University Handbook of Geriatric Medicine
[4] Merck Manual Neurological disorders\Movement and cerebellar
disorders\Parkinson’s Disease
[5] GP Notebook (at
http://www.gpnotebook.co.uk/simplepage.cfm?ID=- 1415970799&linkID=6352&cook=yes)
[6] Kawakami N, Jessen H, Bordini B, Gallagher C, Klootwyk J, Garell CP.
Deep brain stimulation of the subthalamic nucleus in Parkinson's
disease.
WMJ -MADISON , 104(6):35-38 2005
[7] Holroyd S, Currie LJ, Wooten GF. Depression is associated with
impairment of ADL, not motor function in Parkinson disease.
NEUROLOGY , 64(12):2134-2135 2005
[8] Kremer J, Starkstein E. Affective disorders in Parkinson's disease.
International review of psychiatry , 12(4):290-297 2000
[9] Goetz CG, LeWitt PA, Weidenman M. Standardized training tools for the
UPDRS activities of daily living scale: Newly available teaching program.
MOVEMENT DISORDERS , 18(12):1455-1458 2003
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EBM – Parkinson’s Diseases
Version: 1 Final
MED/PD~001(b)
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