Parkinson's disease Flashcards

1
Q

What?

A

Idiopathic syndrome of parkinsonism
Progressive neurodegenerative disorder
Caused by degeneration of dopaminergic neurons in substantia nigra

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2
Q

Other causes of parkinsonism

A
Drug-induced
Progressive supranuclear palsy
Multiple system atrophy
Post-encephalitis
Dementia pugilistica (secondary to chronic head trauma eg boxing)
Toxins: carbon monoxide, MPTP
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3
Q

Drugs causing parkinsonism

A

Note: quicker onset and bilateral
Phenothiazines: e.g. chlorpromazine, prochlorperazine
Butyrophenones: haloperidol, droperidol
Metoclopramide

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4
Q

Epidemiology and risk factors

A
Mean age diagnosis 65
M>F
Increasing age
Pesticide exposure
(???born in spring)
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5
Q

Cardinal triad

A

Tremor
Increased tone (cogwheel rigidity)
Bradykinesia/hypokinesia

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6
Q

Tremor characteristics

A

Worse at rest
Pill-rolling
Brought out with distractability
NOTE: Essential tremor = symptomatic postural and action tremor of arms and head

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7
Q

Bradykinesia characteristics

A

Slow to initiate movements
Slow, low amplitude excursions in repetetive actions (reduced blink rate, monotonous hypophonic speech, micrographia)
Gait: Reduced arm swing, festinance (shuffling, flexed trunk), freezing at obstacles/doors
Hypomimesis (expressionless face)

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8
Q

Presentation

A
Asymmetrical
Bradykinesia plus one or more of: rest tremor, postural instability, rigidity
Other:
Poor decoding of emotional content of speech
Poor executive function
REM sleep disorders
Reduced sense of smell
Constipation
Visual hallucinations
Frequency/urgency
Dribbling saliva
Depression/dementia
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9
Q

Examination

A

Walk, including turn
Upper limb motor exam - ITPRC
Also: reduced amplitude, distraction for rigidity and tremor

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10
Q

Referral

A

Urgently, without treatment if PD suspected
Should be seen w/in 6 weeks if mild
Within 2 weeks if later disease/more complex problems

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11
Q

Investigations

A

Diagnosis is clinical. Investigations are to exclude other causes of parkinsonism
CT/MRI: if fail to respond to L-dopa for 12 weeks; MRI to exclude rare secondary causes (supratentorial tumours, normal pressure hydrocephalus) and extensive subcortical vascular pathology
DaTscan

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12
Q

Conservative management

A

MDT: parkinson’s specialist nurses, physiotherapist, OT, SALT
Refer early (before treatment)
Regular access to specialist care (every 6-12 months)
Good communication between primary and secondary care
Regular assessment of disability (patient self-reporting and objective rating of motor symptoms - Unified PD rating scale)
Consider common non-motor symptoms - sleep disturbance, cognition, depression, psychosis
Education
Nursing assessment
Carer support and involve carers as much as possible
Health and social care assessment
Patient should inform DVLA and insurers

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13
Q

Drug treatments

A

No universal first choice drug
Choice depends on balance of improving motor disability (better with levodopa) vs risk of motor complications (more common in younger people) and neuropsych complications (more common in older/cog impaired patients, more common with agonists)
Options: monoamineoxidase B inhibitors, dopamine receptor agonists, levodopa, amantidine or an anticholinergic

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14
Q

Dopamine agonists

A

Pramipexole, ropinirole, roitigotine
Recommended as initial treatment in younger patients - fewer dyskinesia and motor fluctuations than levodopa
Can be used in early disease
Less effective than levodopa - LD eventually required
Adverse effects (N+V) more common and severe than LD
Can be added to LD to improve motor flucations/reduce LD dose but increased dopaminergic AEs and dyskinesia
Non-ergot derived preferred (pramipexole and ropinirole)
Ergot-derived - NOT first line (fibrotic reactions) (bromocriptine, cabergoline, lisuride, pergolide) - must check renal function, ESR and CXR
SE: impulse control disorders, excessive daytime somnolence, hallucinations in older people, nasal congestion, N+V, postural hypotension

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15
Q

Levodopa

A

Given combined with dopa-decarboxylase inhibitor - prevents peripheral conversion to dopamine. Sinemet and madopar most common
Well tolerated, acute AEs rare and mild
Longer-term: motor complications (dyskinesias), “on-off” (dyskinesias to immobility in a few mins) effect, dry mouth, anorexia/weight loss, palpitations, postural hypotension, psychosis, drowsiness
Reduced effectiveness with time (2 years)

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16
Q

MAOIs

A

Selegiline, Rasagiline
Early treatment with selegiline can delay need for levodopa
Inhibits breakdown of dopamine released by dopaminergic neurons

17
Q

Amantidine

A

?mechanism, probably increased dopamine release and inhibits uptake
SEs: ataxia, slurred speech, confusion, dizziness, livedo reticularis

18
Q

COMT - Catechol-O-Methyl Transderase - inhibitors

A

Entacapone, tolcapone
COMT is an enzyme involved in breakdown on dopamine
Adjunct to LD therapy in established PD

19
Q

Antimuscarinics

A

Procyclidinem benzotropine, trihexyphenidyl (benzhexol)
Block cholinergic receptors
For drug induced parkinsonism more than PD
Help tremor and rigidity

20
Q

Managing wearing off phenomenon

A
Add in/adjust dose of DA/MAOI/COMT inhibitor
Smaller, more frequent doses of LD
Prolonged release LD (before bed)
Take LD 30 min before food
Liquid carbidopa for sever fluctuations
21
Q

Managing on-off fluctuations

A

Combine LD with DA
Fewer doses of LD with SC apomorphine
Liquid LD (closer dose titration)
Diet: small snacks and one large evening meal

22
Q

Managing dyskinesias

A

At peak dose (usually choreic): more frequent, smaller doses of LD (same total daily dose); add long acting DA; slow-release or liquid LD; consider surgery
At beginning/end of dose: try soluble LD before meals; add COMT inhibitor

23
Q

Managing depression in PD

A

Common in PD. Must differentiate from dementia
TCAs or SSRIs
TCAs: if sleep pattern disturbed
SSRIs: if apathy predominant (but don’t use if selegiline used)
Psychotherapy and support groups for patient and carers

24
Q

Managing dementia in PD

A

Cholinesterase inhibitors (eg donepezil, rivastigmine)

25
Q

Managing compulsive behaviours

A

DAs may give compulsive behaviours
Must make patient and carers aware of this
Drugs reviewed by PD specialist if this occurs

26
Q

Managing hallucincations, psychosis

A

May be related to dopaminergic therapy, PD dementia or other confusional state - not necessarily PD related!
Consider gradual withdrawal of PD drugs
Poor prognosis, high mortality
Management difficult, often need nursing home
Do not use typical antipsychotics - only atypicals

27
Q

Acute akinesia

A

AKA Parkinson’s crisis
Rare, life-threatening
Sudden worsening of motor symptoms and severe akinsesia
Triggers: infection, sugery, GI disease, med changes
Difficult to treat, often requires admission

28
Q

Surgical options

A

Pallidotomy - improves motor and ADLs, high side effects
Thalamic surgery - controls tremor, no effect on bradykinesis
Subthalamic surgery: improve tremor, bradykinesia and rigidity, may provoke dyskinesia and hemiballismus
Deep brain stimulation: may reverse rigidity, akinesia and tremor, SEs: intracerebral haemorrhage and confusion; only after drug treatment has failed