This is an HTML version of an attachment to the Freedom of Information request 'LIMA Evidence Based Medicine (EBM)'.

 
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EBM – Parkinson’s Diseases 
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MED/PD~001(b) 
 
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Version history 
Version Date 
Comments 
1e (draft) 
30 March 2007 
Comments from customer incorporated 
1d (draft) 
22 January 2007 
Formatting 
1c (draft) 
18 December 2006 
External review by Dr A Jackson 
1b (draft) 
30 November 2006 
Internal QA by Dr A Ferguson, Dr C Traquair 
and Dr G Buchanan 
1a (draft) 
 
Initial Draft 
 
 
 
Changes since last version 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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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 

 
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 

one arm definitely decreased in amount of  1 
swing 
one arm fails to swing 

both arms fail to swing 

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 

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 

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 

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 

  
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   
 
[10]  Zi‚gler M, Broucker T De, Damier P, Humbert R, Clerson P,  
        Richard-Berthe C.  Handipark: A simple test of the impact of                          
Parkinson's disease on activities of daily living. 
        Revue neurologique ,   159(8-9):767-774 2003    
 
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