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parkinson's Flashcards

1
Q

what is parkinson’s

A

progressive idiodegeneration of the dopaminergic pathways in the substantia nigra

loss of dopaminergic neurones in the substantia nigra that leads to inadequate dopamine transmission.

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2
Q

characteristic neuropathological finding

A

lewy body formation in affected neurones

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3
Q

gold standard for diagnosis for parkinsons

A

brain bank criteria

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4
Q

brain bank criteria for the diagnosis of Parkinson’s disease

A

step 1:
clinical syndrome involving bradykinesia (+rigidity important

plus at least one of

  • tremor - 4-6 Hz - corase, pill-rolling, disappears during voluntary movement, asymmetrical
  • rigidity
  • postural instability

step 2: exclude other potential conditions

step 3
PLUS 3 OR MORE

  • Unilateral onset
  • stooped posture
  • loss of arm seing
    • Rest tremor present
    • Progressive disorder
    • Persistent asymmetry affecting side of onset most
    • Excellent response (70-100%) to levodopa
    • Severe levodopa-induced chorea
    • Levodopa response for 5 years or more
    • Clinical course of ten years or more
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5
Q

Other parkisonian features apart from the triad

A
  • Depression, anxiety, and fatigue.
  • Reduced sense of smell.
  • Cognitive impairment.
  • Sleep disturbance.
  • Constipation.
  • lack of facial expression
  • lsck of spontanrous movements
  • greasy skin - autonomic dysfunction
  • decreased blinking
    tibulation - nodding head involuntarily
  • dribbling of saliva
  • festinating gait
  • stooped posture
  • increased tone
  • impotence
  • sweating
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6
Q

what is lead pipe rigidity

A

constant resistance felt when a limb is passively flexed in the presence of increased tone without tremor,

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7
Q

what is cogwheel rigidity

A

regular intermittent relaxation of tension felt when a limb is passively flexed in the presence of tremor and increased tone.

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8
Q

what may be seen when examining a parkinson patient

A

reduced facial expression
slow
shuffling, festinating gait

pill rolling
‘pull test’ - tendency to fall back when pulled by examiner

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9
Q

other causes of parkinsonism

A

drug-induced parkinsonism

antipsychotics
antiemetics
- prochlorperazine
- metocloperamide

amiodarone
antidepressants - SSRIs

wilson’s
repeated head injury
cerbrovascular disease

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10
Q

other causes of tremor

A

1) essential tremor
- bilateral stress, caffeine, sleep deprivation

exaggerated psychological tremor

dystonic tremor

hyperthyroidism

drugs - B2 agonists

2) intention - cerbellar

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11
Q

name of scales used to assess progression of parkinson

A

Hoehn and Yahr

Unified Parkinson’s Disease Rating Scale

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12
Q

classification of Unified Parkinson’s Disease Rating Scale

A

Part 1: non-motor experiences of daily living
Part 2: motor experiences of daily living
Part 3: motor examination
Part 4: motor complications

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13
Q

drugs available for parkinson

SEs

A

levodopa - pass thru BBB - converts levodopa into dopamine

neuroepileptic malignant syndrome

monomine oxidase B inhibitors - dizzy, insomnia, orthostatic hypotension, joint pain

and COMT - coloured urine, diarrhoea, liver damage, impulsive and compulsive behaviours

stop breakdown of dopamine

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14
Q

4 phases of parkinson

A
  1. Early stage - Soon after diagnosis, symptoms are mild and normal life possible
  2. Maintenance stage - Good response to treatment and no major disability
  3. Advanced stage - Poor response to drugs with motor side effects
  4. Palliative stage - Unable to live independently and in need of multidisciplinary support
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15
Q

clinical features of vascular pseudoparkinsonism

A
  • bilateral symmetrical rigidity;
  • bradykinesia, predominantly involving - lower limbs
  • postural instability; shuffling gait
  • falls;
  • dementia
  • corticospinal findings.
    resting tremor maybe absent
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16
Q

clinical features of benign essential tremor

A

Begin gradually, usually more prominently on one side of the body

Worsen with movement
Usually occur in the hands first, affecting one hand or both hands

Can include a “yes-yes” or “no-no” motion of the head

May be aggravated by emotional stress, fatigue, caffeine or temperature extremes

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17
Q

dementia with lewy bodies

A

cognitive symptoms develop within the year whereas IPD is after a year

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18
Q

features of progressive supranuclear palsy

A

postural instability and falls
— patients tend to have a stiff, broad-based gait

impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)

parkinsonism
— bradykinesia is prominent

cognitive impairment
— primarily frontal lobe dysfunction

pseudobulbar palsy

supranuclear opthalmoplegia

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19
Q

progressive supranuclear palsy ?

A

brain cells in certain parts of the brain are damaged as a result of a build-up of a protein called tau

20
Q

features of multiple system atrophy

A

alpha synuclein build up

parkinsonism + autonomic disturbance

  • erectile dysfunction: often an early feature
  • postural hypotension
  • atonic bladder

POOR RESPONSE TO LEVODOPA

  • rapid progression
  • pronounced autonomic failure

cerebellar signs

autonomic NS affected

bladder problems
low BP

Problems with co-ordination, balance and speech
slow moving and feeling stiff

21
Q

types of multiple system atrophy

A

1) MSA-P - Predominant Parkinsonian features

2) MSA-C - Predominant Cerebellar features

22
Q

first line treatment for parkinson

A

if the motor symptoms are affecting the patient’s quality of life: levodopa

if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

23
Q

impulse control disorders more significant

features

A
  • dopamine agonist therapy
  • a history of previous impulsive behaviours
  • a history of alcohol consumption and/or smoking
24
Q

SEs of levodopa

A

dyskinesia (involuntary writhing movements), ‘on-off’ effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness

25
Q

what happens if you stop levodopa acutely

A

acute dystonia

26
Q

examples of dopamine receptor agonists

A

bromocriptine, ropinirole, cabergoline, apomorphine

27
Q

SEs fo dopamine receptor agonists

A

(bromocriptine, cabergoline) have been associated with pulmonary, retroperitoneal and cardiac fibrosis.

impulse control disorders

excessive daytime somnolence

more likely to cause hallucinations comapred to levodopa

nasal congestion
postural hypotension

28
Q

examples of monoamine oxidase B inhibitors

A

e.g. selegiline

inhibits the breakdown of dopamine secreted by the dopaminergic neurons

29
Q

SEs of amantadine

A

ataxia, slurred speech, confusion, dizziness and livedo reticularis

30
Q

COMT eg

A

entacapone, tolcapone

COMT is an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy

31
Q

antimuscarinics?

A

block cholinergic receptors
now used more to treat drug-induced parkinsonism rather than idiopathic Parkinson’s disease
help tremor and rigidity
e.g. procyclidine, benzotropine, trihexyphenidyl (benzhexol)

32
Q

DDx fro parkinson

A

vascular pseudoparkinsonism
benign essential tremor

parkinsonism + syndromes

drugs
antipsychotics
toxins - CO, MPTP

depression

33
Q

What is meant by on/off fluctuations in patients who are taking levodopa
preparations and why do they occur?

A

Unpredictable fluctuations in motor function due to “wearing off”.

34
Q

causes of parkinsonism

A 
Parkinson's disease
drug-induced e.g. antipsychotics, metoclopramide*
progressive supranuclear palsy
multiple system atrophy
Wilson's disease
post-encephalitis
dementia pugilistica (secondary to chronic head trauma e.g. boxing)
toxins: carbon monoxide, MPTP
35
Q

excessive daytime sleepness remedy

A

modafinil reviewed every 12 months

cant drive infrom DVLA

36
Q

orthostatic hypotension remedy

A

midodrine hydrochloride

then
fludrocortisone acetate

37
Q

drooling of saliva

A

glycopyrronium bromide

2nd line botulinum toxin A

38
Q

Managing motor Sx of parkinsons

A

offer levodopa w carbedopa or benserazide in early stages of parkinson’s disease whose motor Sx impact their quality of life

QOL not affected OFFER levodopa, non-ergot-derived dopamine-receptor agonists (pramipexole, ropinirole or rotigotine) or monoamine-oxidase-B inhibitors (rasagiline or selegiline hydrochloride).

ADJUVANT THERAPY
Patients who develop dyskinesia or motor fluctuations despite optimal levodopa therapy should be offered a choice of
- non-ergotic dopamine-receptor agonists (pramipexole, ropinirole, rotigotine)
- MAOI (rasagiline or selegiline hydrochloride)
- COMT inhibitors (entacapone or tolcapone) as an adjunct to levodopa.

ergot-derived dopamine-receptor agonist (bromocriptine, cabergoline or pergolide) should only be considered as an adjunct to levodopa if symptoms are not adequately controlled with a non-ergot-derived dopamine-receptor agonist.

If dyskinesia is not adequately managed by modifying existing therapy, amantadine hydrochloride should be considered.

39
Q

What info should be given when starting Mx for motor Sx

A

impulse control disorders esp w dopamine agonists

excessive sleepiness

sudden onset of sleep w dopamine agonists

Psychotic Sx THESE 3 Sx more likely to be seen with dopamine receptor agonists

Levodopa treatment is associated with motor complications, including response fluctuations and dyskinesias. Response fluctuations are characterised by large variations in motor performance, with normal function during the ‘on’ period, and weakness and restricted mobility during the ‘off’ period.

40
Q

Long term problems of parkinsons

A

50-90% of people who have received L-dopa for 5-10 years may experience the following

  • motor fluctuations-> when the dose is wearing off, “on” may experience involuntary movements DYSKINESIAS
  • Axial problems are balance, speech and gait disturbance which do not respond to Parkinson’s disease medication -> Due to degeneration outside the substantia nigra where dopamine is not the NT -> Mx- SALT and physio, OT

Parkinson’s dementia -> occurs more than one year after diagnosis of Parkinson’s

  • Presence of Parkinsonism in the limbs.
  • Frequent visual hallucinations.
  • Frequent fluctuations in lucidity.
41
Q

Mx of nocturnal akinesia

A

levodopa or oral dopamine-receptor agonists should be considered

2nd line -> rotigotine

42
Q

Mx of psychotic Sx

A

No CI -> quetiapine to treat hallucinations and delusions.

above ineffective -> clozapine offered

43
Q

Mx of rapid eye movement sleep behaviour disorder

A

clonazepam

melatonin

44
Q

Mx of advanced parkinson’s disease

A

apomorphine hydrochloride w domperidone if they ahve N/V

chech ECG due to cardiac effects

deep brain stimulation - IF DRUG DO NOT WORK

45
Q

what is impulse control disorders

A

compulsive gambling, hypersexuality, binge eating, or obsessive shopping

on dopaminergic therpay

modify Mx

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