Transcript Parkinson`s Disease - Pennine GP Training

Management of parkinson’s
disease.
Dr. Sanjiv Chandratre.
Consultant in med. for elderly 2010
What you should expect from this
teaching session.
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How to diagnose PD.
What is the D/D of PD
How to treat PD ( Medical treatment.)
When to refer pts to secondary care.
Tricks of the trade in managing special problems
related to PD.
• What services are available in our area for PD
patients.
• Nice guidelines on PD and results of our audit.
James parkinson 1817
• Involuntary tremulous motion, with
lessened muscular power, in part not in
action and even when supported;with a
propensity to bend the trunk forward, and to
pass from a walking to a running pace: the
senses and intellect being uninjured.
Terminology in P. D.
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Parkinson’s disease or Idiopathic P. D.
Parkinsonism / Parkinsonian syndrome.
Drug induced Parkinsonism.
Post encephalitic parkinsonism.
Vascular pseudo Parkinsonism.
Lower body parkinsonism.
Terminology in P. D.
• Parkinsonism plus syndrome.
– PSP
– MSA
– CBD
Parkinson’s disease
• Progressive, disabling and distressing
• Appropriate management and planning right
from the start can prevent some of the most
distressing features
• Team work can solve most of the problems
and can help deliver better care cost
effectively
• The 4 stages….
4 stage clinical management
scale
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Diagnosis
Maintenance therapy
Complex
Palliative care
Incidence and Prevalence
• Incidence
• Number of new cases
in a population,
usually /100,000
• Around 11 per
100,000
• Prevalence
• Total number of
people in a population
with the condition,
• I.e.cumulative
incidence per annum
minus deaths.
• Around 100- 200 per
100,000
Prevalence
• Per GP.
• Say 2500
• Per district / pct.
• Say 200,000
Brain Bank Criteria
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Step 1
Diagnosis of parkinsonian syndrome
Step2
Exclusion criteria for IPD
Step3
Supportive criteria for IPD
Step1- Diagnosis of parkinsonian
Syndrome.
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Bradykinesia +at least one of the following
Muscular rigidity
4 –6 Hz resting tremor
Postural instability
Brady / Hypokinesia
• Hypokinesia –poverty of movement
• Loss of facial expression, arm swing,
gesture etc.
• Bradykinesia -Slowness of movement
• ‘Decay’ – finger/ heel tap
Rigidity
• Resistance to passive movement
– Reinforcement – ‘froment’s manoeuvre’
• Constant [ c. f. ‘clasp-knife’]
– ‘Lead pipe’
– ‘cogwheel’
• Gagenhalten
Tremor
• Involuntary rhythmical alternating
movement
• Begins unilaterally – upper limb
• 4 – 6 hertz, ‘pill rolling’
• First symptom in 75%
• - 20 % never develop it
• Postural tremor can also occur
Postural instability.
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Last cardinal feature to appear
Limited diagnostic specificity in the elderly.
Pull test
Early falls – ‘red flag’
Step 2 – exclusion criteria
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History of repeated strokes.
History of repeated head injury.
History of definite encephalitis.
Cerebellar signs.
Early severe autonomic involvement
Supranuclear gaze palsy
Neuroleptic drugs
Negative response to large doses of levodopa
Step3- positive supportive criteria
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[>3 for ‘definite’ PD ]
Unilateral onset.
Rest tremor
Progressive
Persistent asymmetry
Excellent levodopa response
Severe levodopa induced chorea
Levodopa response>=5years
Clinical course>=10 years
Diagnosis- Accuracy
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Meara 1999 Age and ageing
Community study- 402 cases
73 % Parkinsonism
53% ‘probable’ IPD
Essential tremor
Alzheimer’s disease
vascular
Accuracy of diagnosis
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Brain bank post mortem series
24 % error rate.
10 % latest studies.
2% MD specialists.
• Community series
• >50 % error rate
Is the diagnosis correct?
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Diagnosis of P. D. can be very difficult.
There is no diagnostic test.
Diagnosis is made clinically.
DAT scan of limited value.
Error rate is high. 25 % in the hands of
neurologist. Upto 50 % in the community.
• F.U. and review of diagnosis is important.
Dopamine Transporter Imaging agent
•Parkinson’s disease
•Progressive Supranuclear
Palsy
•Multiple System Atrophy
•Essential Tremor
•Neuroleptic-induced
Parkinsonism
•Vascular disease
Differential diagnosis of
parkinsonian syndrome
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Idiopathic Parkinson’s disease
Drug induced – phenothiazines
Multiple cerebral infarct state.
Trauma – pugilistic encephalopathy
Toxin induced- MPTP, CO, Mn, Cu,
Parkinson’s plus syndromes
Essential tremor
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Most common diagnostic error.
10 times more common than PD.
Postural or action tremor.
Titubation.
Family history.
B – Blockers help.
Drug induced parkinsonism.
• Causes
– Predictable
Neuroleptic drugs (both typical and atypical)
Hidden neuroleptics- metoclopromide,
prochlorperazine
Combination with antidepressants( fluphenazine )
Calcium antagonist
--Idiosyncratic
Lithium, sodium valproate, amiodarone
mainly tremor but parkinsonism reported.
Multiple infarct state
• Synonymous with leucoariosis,
Binswanger’s encephalopathy
• Related to hypertension and other risk
factors
• Common misdiagnosis.
• Poor prognosis
• Aspirin and dipyridamole retard may be
effective and safe
Vascular parkinsonism
• PM studies 2-3 %incidence of ‘pure’
vascular causes
-no lewy bodies or nigral degeneration
Acute or abrupt onset
basal ganglia infarct
Insidious progression
Diffuse sub cortical white matter ischaemia.
Dementia with Lewy bodies
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Fluctuating alertness
Hallucinations
Mild parkinsonism
Neuroleptic sensitivity
• Tremor less common
• More symmetrical
• Myoclonus more
common
• More rigid, less
bradykinetic
Medical treatment of P. D.
Only 18 drugs for PD in BNF 2008
14 Dopaminergic
4 Anticholinergic.
Drugs to avoid 1
• Antiemetics
– Metoclopromide (Maxalon)
– Prochlorperazine (Stemetil)
• The only recommended antiemetics are
– Domperidone
– 5ht3 antagonists eg. Ondensetron.
Drugs to avoid 2
• Antipychotics
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Chlorpromazine
Sulpride
Haloperidol
Thioridazine.
• Newer antipsychotic can be used with
caution
When to start treatment ?
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Controversial
Is the diagnosis certain.
Age of patient.
Effect on ADL.
Patient Choice.
Drugs in PD
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Levodopa preparations.
Dopamine receptor agonists.
Monoamine oxidase-B inhibitors.
Catechol-o-methyltransferase inhibitors.
Anticholinergics.
Amantadine
Levodopa
• Used since the 1960’s
• Remains the ‘gold standard’
• Always used with dopa decarboxylase
inhibitor.( either carbidopa or benserazide.)
• Side effects are common.
Levo dopa preparations.
• Madopar or co beneldopa—Levodopa with
benserazide
• Sinemet or co careldopa—Levodopa with
carbidopa
Levodopa formulations
• Effervescent or dispersible eg. Madopar
dispersible.
• Conventional release.eg. Madopar
• Controlled release.eg. Madopar CR or
Sinemet CR
• Duodopa– As a gel.
Levodopa preparations
• Dispersible preparations—Use for morning
kick start or for on off fluctuations. Also in
patients with swallowing difficulties.
• CR preparations– unpredictable absorption.
Use now mostly at night for nocturnal
symptoms like difficulty turning in bed or
AM dystonias
Side effects of levodopa
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Very common
Nausea, vomiting
Excessive drowsiness
Insomnia
End of dose fluctuations.
Nocturnal immobility.
Motor fluctuations and dyskinesias.
Dopamine agonists
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First available since 1970’s
Six DA’s available for oral use.
Apomorphine administered parenteraly
Act directly on post synaptic receptors.
Two types
– Ergot derived.
– Non ergot derived.
Dopamine agonists
• ERGOT
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Bromocriptin
Lisuride
Pergolide
Cabergoline
• Non ERGOT
– Ropinirole
– Pramipexol
– Apomorphine.
Rotigotine
• DA
• Mono therapy or adjunct.
• Patches.
Side effects of DA’s
• Similar to levodopa
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Nausea.
Vomiting.
Postural hypotension.
Confusion.
Hallucinations.
Somnolence.
Side effects of ERGOT DA’s
• Fibrotic reactions.
• Pulmonary, retroperitoneal and pericardial
fibrosis.
• Cardiac valvulopathy.
• In most cases non ergot DA’s preferred.
• CXR, PFT’s, ESR,and S. creatinine before
starting treatment.
Unusual side effects of DA’s
• Complex group of impulse control disorders
– Pathological gambling.
– Hypersexuality.
– Compulsive eating or shopping.
. Repetitive perseverative behavior.
-- Punding
-- Excessive hobbyism.
Unusual side effects of DA’s 2
• ‘Dopamine dysregulation syndrome’
– Compulsive use of increasing doses of
levodopa
• ‘hedonistic homeostatic dysregulation
syndrome’.
• 14% prevalence of ICD.
• Eight fold increase in those taking DA’s
• Young pts. are particularly prone.
SOOS
• Excessive day time sleepiness and soos can
occur with levodopa preparations and with
DA’s
• Warn patients about driving.
Amantidine
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Antiviral properties.
Weak DA
Only for moderate to severe dyskinesia.
Glutamate antagonist.
100 mg. BD or TDS
COMT inhibitors
• Entacapone
• Talcapone
• In combination with levo dopa
– ( STALEVO)
Stalevo
• Combination of Levodopa, carbidopa and
Entacapone.
• 50 mg./12.5 mg./200 mg.
• 100 mg./25mg./200mg.
• 150 mg./37.5mg./200 mg.
• 200 mg./50 mg./ 200 mg.
MAO -B inhibitors
• Selegiline
– 10 mg. Od or 5 mg. Bd
– 2.5 mg in elderly.
– Zelapar( oral lyophilisate ) 1.25 mg. Before
breakfast. Place on tongue and allow to dissolve
– Neuroprotective??
• Rasagiline
– 1 mg.
Expensive.
Antimuscarinic drugs.
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Benzatropine, Procyclidine,Orphenadrine
Limited use.
Cognitive impairment in elderly.
Useful in drug induced Parkinsonism.
can be used for excessive salivation.
Apomorphine
• Potent dopamine agonist.
• Significant cost (10,000 £ PA for cont.
infusion.) offset by keeping pts. Out of
NH’s
• Only parenteral use.
– Subcutaneous (rescue ) injections.
– SC continuous infusion.
Apomorphine.
• Severely emetogenic.
• Needs priming with Domperidone.
• Only used in advanced PD with severe
motor fluctuations.
• Injection site reactions.
• Could be an alternative to invasive surgical
procedures.
DO NOT MISS P. D.
MEDICATION
• Akinetic Rigid Syndrome.
• Malignant neuroleptic syndrome.
• ‘GET IT IN TIME’
Non motor symptoms in P. D.
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Constipation
Hallucinations.
Dementia / psychosis.
Excessive salivation.
Excessive sleep.
REM behaviour disorders.
P. D. and Driving
• Booklet from PDS.
• Diagnosis of P. D. does not necessarily
disqualify people from driving
• Dopamine agonists– Drowsiness
– SOOS
Do I have to inform DVLA
Yes.Required by law.
Drivers medical unit at DVLA
Criminal offence under RTA 1988
Take home messages
• Diagnosis of PD is clinical and can be difficult.
• Every patient should be referred to secondary care
to confirm the diagnosis and initiate treatment
• Treatment should only be started if there is
functional impairment
• Levodopa is the gold standard but DA cause much
less diskinesia
• Follow up should be life long
Thank you.
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ANY QUESTIONS ?
Outline
1. History
2. Diagnosis
3.Differential diagnosis
4.Cost factors
5. Local scene
6. Take home messages
Historical aspects
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James parkinson [ 1755- 1824] 1817
Charcot - ‘la maladie de parkinson’
Lewy [1921]
Carlson [1958]
Birkmayer, Hornykiewicz [1961]
Cotzias [1967]
Hoehn and yahr [1967]
Why is diagnosis of PD and
parkinsonian syndromes challenging?
• Diagnosis is clinical
• Presence and progression of clinical features
Supportive for PD
Atypical for PD “ Red ”flags
• Most difficult in early stages
• Large number of imitators of PD
• Co morbidity and confounders increase with age
• Tremors, shaking
• Gait disorders
• Slowness and true bradykinesia
Diagnostic Challenges
• Prevalence of Signs of Parkinsonism in the “Normal”
Elderly Population
• Co-existent Pathology
– Cerebrovascular Disease
– Depression
– Arthritis
• Differential Diagnosis
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Essential Tremor
Parkinson’s Plus Syndromes
Alzheimer’s
Lewy Body Disease
Challenge tests
• Oral levodopa/ subcutaneous apomorphine
• False positives [e. g. M.S.A.] and false
negatives
• Lowest sensitivity / specificity in early
disease
• Not recommended routinely
• ‘Priming’
Cost Overview
• Direct Costs
• Indirect Costs
• TOTAL = Direct + Indirect
NHS
Social services
Private Expenditure
(Financial Benefits)
Lost earnings
OR
Lost leisure time
OR
Carer replacement cost
Total Cost of PD Care 1994
£382,705
£, 000
%
•Out-patient
19,147
5
•Drugs
26,900
7
•Hospital In-patients
49,386
13
•Home Care
107,915
28
•Residential Home
179,358
47
Conclusions: PD Economic Impact
(1)
• Parkinson’s Disease is an expensive condition
• The greatest single costs relate to lost earnings in younger
patients; long term institutional care in older patients
• Mean direct costs per patient is inversely proportional to
age:
• c£4,000 per annum below 65 years
• c£9,400 per annum over 85 years
• Mean direct annual costs is inversely proportional to
disease severity
• Hoenhn & Yahr stage (0-1) c£3000
• Stage 5 c£18,400
• Greater than five fold increase
Previous Cost Estimates (2)
• “Moving and Shaping” PDS, 1999
Estimated costs of PD
£ 3,500-10,000 per patient
£7-20,000 per GP
£560,000-£1.6m per PCG
• Dodel 2000 MoDis (Barcelona)
• Nuijten Oct. 2000 EFNS
– 50,000 Euro in 5 yrs (£6k pp/pa)
– model used in justification of additional drug cost
What can we except in the near
future?
• Neuroprotective agents. – Problems in trial
designs.
• Continuous dopaminergic stimulation.
Rotigotine patch,once daily formulations of
pramipexol and Ropinirole.
• Neurorestoration- Stem cell implants, Nerve
growth factors
Conclusions: the Economic Impact
(3)
• Within NHS costs, the split between
primary care (incl drugs) and secondary
care is roughly equal across age groups.
• However, across H&Y stages secondary
care accounts for an increasing proportion
(27% in stages 0-1, 62% in stage V)
Case history 1
complex phase IPD
• A.L. 65 yrs. M
• Nov 02 .ref. by Dr omer( previously under Dr.
Loisou )
• P. D. 12 yrs.
• Severe Dyskinesia– End of dose? Random?
• On madopar, selegeline , Ropinirole and
dispersible madopar
• Could not tolerate Entacapone
• Ref. to Leeds ( Dr. spokes ) after I. P. stay
Case history 1( contin.)
• Decided to admit to LGI for trial of apomorphine
• 20 weeks in LG
• Aspiration pneumonia—ITU—VentilatedTracheostomy—PEG.—back to CRH
• Refused RH/ NH. Very dependent. Huge package
of care.----Home.
• Managed for 5 months. Readmitted with
aspiration pneumonia
• Died.
Average total life expectancy
[ uk 1999]
• Age
Male
Female
0
75.1
75.1
80.0
80.0
30
46.4
76.4
50.8
80.8
60
19.2
79.2
22.8
82.8
85
6.9
91.9
8.6
93.6
European Parkinson’s Association
and WHO charter of rights for
people with PD
• People with Parkinson’s have the right to:
• Be referred to a doctor with a special interest in
Parkinson’s
• Receive an accurate diagnosis
• Have access to support services
• Receive continuous care and
• Take part in managing the illness
Declared on this day the 11th day of April 1997
Case 2
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H.J. 80 m . Rtd. Bank manager
With wife, slight confusion
Fully compesmentis
No evidence of P.D.
All investigations- NAD
9mths later---review
Restless and agitated at night ,paranoid
Walked slowly
Case 2 (cont.)
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No definite evidence of P.D.
??parkinson plus syndrome
Ref. to Dr.. Orange
Admitted– v. hallucinations.
Confused, fluctuating cognition, hypomimia
Pill rolling tremor--Rapid deterioration
Needed N.H.
case3
• H.B. 84 M , lives with wife at Hebden bridge. On
holiday– adm. To hospital in Lancashire– chest
infection. Started on madopar--- “lack of facial
expression”
• Transferred to CRH
• Not convinced with diagnosis of PD
• Madopar stopped.
• No change
• F. u. in opd
Case 1 – GP’s Letter
Please see this 62 year old man with a 6 year history of an
upper limb tremor. This interferes with eating and is a
considerable embarrassment to him.
I thought this was Parkinson’s Disease and gave him Sinemet
Plus 1 tds but there has been no response.
I am not sure what is wrong with him and would value your
advice.
Case 1 – GP’s letter
• What is the most likely diagnosis and why?
• What is the relevance of the duration of the
history?
• What is the relevance of the physical type
of tremor and the trouble it is causing?
• Is the lack of response to Levodopa
relevant?
Case 1 – Your history & examination
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6 years – progressive – postural & action tremor
Main problem with teacups and spoons
No regular medication
Brother has similar tremor
Symmetrical upper limb postural and action
tremor
• No features of Parkinson’s Disease
Case 1 – Your history & examination
• What is the diagnosis now?
• What is the relevance of the drug history?
• What is the relevance of the family history?
• Is this type of tremor always symmetrical?
Case 1 – Conclusions
• Diagnosis – Essential Tremor
• Note duration, tremor with posture / action, family
history and lack of response to Levodopa
• Beware Beta-agonist Inhalers for asthma
• Response to Ethanol
• Can effect head (titubation) and voice
• Prevalence – 10 times more common than P.D.
Case 1 - Conclusions
• Treatment
• None
• Propranolol LA – 80 mg/d for one week then 80 mg bd. No better in 2
months – 80 + 160 mg/d then another 2 months 160 mg bd.
• Primidone Syrup (250 mg/5 ml) – 125 mg/d increased at weekly
intervals by 125 mg/d depending on response and tolerance
• Other anti-epileptic drugs can be tried such as Gabapentin and
Topiramate
• Botulinum toxin into forearm muscles controlling wrist action – must
be repeated at 3 monthly intervals
• Bilateral thalamic stimulation if very debilitating
Case 2 – GP’s Letter
This 82 year old man was diagnosed with Parkinson’s Disease by Dr X
last year. He has not responded to Sinemet and his wife would like an
expert opinion.
His gait has deteriorated over the last few years and now he is rather
confused.
He has mild angina and hypertension. He wears an urinary sheath for
incontinence.
The home situation is getting very precarious and the family desperately
need him to be treated effectively.
Case 2 – GP’s Letter
• Has he got Parkinson’s Disease?
• What clinical features does he have?
• What is the most likely diagnosis?
Case 2 – Your history & examination
• 7 year progressive history of:
• Shuffling gait with recent falls
• Cognitive decline with poor short-term memory and
confusion
• Urinary incontinence
• Normotensive on anti-hypertensives
• No ‘cardiac’ signs
• No Parkinsonian features in the upper limbs
• Shuffling gait
• Reflexes marginally brisk with flexor plantar responses
Case 2 – Your history & examination
• What is the most likely diagnosis?
• What are the alternatives?
• What investigations would you do?
• What treatment would you recommend?
Case 2 - Conclusions
• Diagnosis – Multiple Infarct State
• Synonymous with leucoariosis, Binswanger’s
encephalopathy
• Related to hypertension and other risk factors
• Common misdiagnosis!
• Poor prognosis
• Aspirin and Dipyridamole retard may be effective
and safe
Case 3 – GP’s Letter
This 58 year old man has been under the care
of Urologists for many years with renal
stones. His gait over the last year has been
unsteady and he is generally a little slow.
His wife is a nurse and wonders if he has a
neurological disorder. I would very much
value your opinion.
Case 3 – GP’s Letter
• What are the possible diagnoses?
Case 3 – Your history & examination
• 2 year history of tendency to shuffle and general slowness
but no falls or tremor
• Symmetrical bradykinesia and hypokinesia
• Rigidity with reinforcing manoeuvres in both upper limbs
• No tremor
• Reflexes all pathologically brisk with flexor plantar
responses
• Closer questioning reveals impotence for last 4 years
• No postural drop in blood pressure
Case 3 – Your history & examination
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What is the diagnosis?
What are the diagnostic features?
What systems are involved?
What investigations can be performed?
How would you treat him?
Case 4 - Conclusions
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Diagnosis – Progressive Supranuclear Palsy
Systems involved:
Dementia
Ophthalmoparesis – downgaze, then upgaze then
horizontal gaze palsy
Extrapyramidal – Parkinsonism, early falls!
Corticospinal tracts – upper motor neurone signs in limbs
and bulbar musculature (dysphagia)
Miscellaneous – retrocollis
Poorest prognosis – median survival = 7 years
GP suspects PD
GP refers for specialist opinion
Specialist confirms diagnosis
Wait for significant
functional disability
Levodopa
Dopamine agonist
Motor complications
develop
Disease progression
Add small amounts of Levodopa
Motor complications develop
Consider CR Levodopa
Consider agonist
Consider Entacapone
Consider CR Levodopa
Consider Entacapone
Severe motor complications
Consider Apomorphine / Consider Surgery
Fractionate dose of Levodopa
Consider modified-release Levodopa
Add modern Dopamine agonist
Add Entacapone
Consider Apomorphine
Injections or infusions
Consider surgery
Case 4 – GP’s Letter
• What is the likely diagnosis?
• What are the diagnostic features?
Case 4 – GP’s Letter
Thank you for seeing this 56 year old man with
unsteadiness and falls over the last 3 years.
His wife says he is slowing down and mentally is not
as agile as he was. As a result he took early
retirement last year.
He looks as though he has Parkinson’s Disease to me
but I would value your opinion.
Case 4 – Your history & examination
• 3 year history of progressive shuffling gait and falls for the
last 12 months
• Possible dementia
• Normal eye movements and bulbar function
• Parkinsonian facies and rigidity with symmetrical
hypokinesia and bradykinesia
• No tremor
• Very slow unsteady gait with tendency to fall backwards
• Reflexes brisk and plantar responses extensor
Case 3 - Conclusion
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Diagnosis – Multiple System Atrophy
Systems involved:
Extrapyramidal – Parkinsonism
Cerebellar signs – ataxia, intention tremor, nystagmus
Corticospinal tracts – upper motor neurone signs in limbs
Autonomic function – impotence, bladder disturbance, postural
hypotension
Miscellaneous – disproportionate antecollis, laryngeal dystonia
(sudden death)
No dementia!
Intermediate prognosis – median survival = 9 years
Emotional incontinence
Case 4 – Your history & examination
• What is the diagnosis?
• What are the diagnostic signs?
• What systems are involved?
• What investigations can be performed?
• How would you treat him?
Calne classification 1992
• Clinically possible IPD : One of the
following; tremor, rigidity, bradykinesia
• Clinically probable IPD: Two of the
following cardinal features; resting tremor,
rigidity, bradykinesia,or postural instability or if
resting tremor, rigidity, or bradykinesia are
asymmetric
• Clinically definite IPD; three of the cardinal
features or two cardinal features with one of the
first three presenting asymmetrically
Local scene
• PD clinic started 2 nd nov. 04
• PD nurse interviews in feb 05
• PD society in Halifax– very active and has
pledged 52,000£ for pump priming a nurse
post.
• Patients who need apomorphine have to
travel to Leeds
What can we expect in the near
future?
Everything that shakes is not
Parkinson’s…
Dr. S. N. Chandratre.
Consultant Medicine for Elderly.
Calderdale Royal Hospital.
Stages of P. D.
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Diagnostic phase
Maintenance phase.
Complex phase.
Palliative phase.
Drugs used in P. D.
• Dopamine receptor
agonists.
• Levo dopa
preparations.
• MAO B Inhibitors
• COMT Inhibitors.
• Amantidine
Treatment of P. D.
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Medical
Surgical
Complementary
Role of PDNS, OT, Physio, SALT,
Dietetian, SW
Route of administration
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Oral – Effect of meal ?
Sub cuteneous
Skin patch
Effervescent tablets.
Duodopa- via PEG