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Dunedin RACP Study Course > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Clinical diagnostic features for PD

A
  • Rest tremor
  • rigidity
  • Bradykinesia/ Akinesia
    (± postural reflexes decreased - imbalance)

2 of the 3 features are required for diagnosis 1 of the 2 has to be bradykinesia

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2
Q

Definition of bradykinesia (in PD)

A

Slowness of movement AND decrement in amplitude or speed (or progressive hesitations/halts) as movements are continued.

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3
Q

Fatiguing in PD vs non PD movement disorders

A

In parkinsonism caused by PD, a decline in either speed or amplitude is seen as movements are continued, a feature sometimes not observed in parkinsonism caused by alternate conditions.

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4
Q

Non-Motor Sx PD

A
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5
Q

3 stages of early PD

A
  1. Preclinical PD
    - neurodegenerative processes have commenced, but there are no evident symptoms or signs
  2. Prodromal PD
    - symptoms and signs are present, but are yet insufficient to define disease
  3. Clinical PD
    - diagnosis of PD based on presence of classical motor signs
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6
Q

Main RFs for PD

A

Smoking

FHx

Age

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7
Q

Major prodromal features of PD

A
  1. RBD (REM sleep behaviour disorder)
  2. hyposmia
  3. anxiety
  4. constipation
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8
Q

Diagnosis of REM sleep Behaviour Disorder

A
  • movements of the body or limbs associated with dreaming
  • plus at least one of the following:

– potentially harmful sleep behaviour

– dreams that appear to be acted out

– sleep behaviour that disrupts sleep continuity

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9
Q

What are Lewy bodies made of

A

alphasynuclein (alpha-SN) and several other proteins

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10
Q

Anatomical progression of PD

A

advances in an orderly sequence, starting in the medulla and the olfactory bulb, then spreads upwards to substantia nigra, then finally into the cortex

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11
Q

AE of levodopa

A

Nausea
Orthostatic hypotension
Confusion , Hallucinations
Sleepiness and sleep attacks

Motor fluctuations and dyskinesia
Impulse control disorders - worsens

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12
Q

Anti-emetics in PD

A

Use domperidone or ondansetron

Avoi:
metoclopramide, prochlorperazine

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13
Q

Issues with ergot dopamine issues

A

cardiac/lung/retroperitoneal fibrosis

Unavailability

Just use no-ergot derivatives

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14
Q

Nonergot dopamine agonists

A

apomorphine (subcutaneous)
pramipexole
ropinirole
rotigotine (transdermal)
piribedil

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15
Q

Dopamine agonist AE

A

Nausea
Orthostatic hypotension
- worse than with

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15
Q

Dopamine agonist AE

A

Nausea
Orthostatic hypotension
- worse than with levodopa
Confusion and hallucinations
Sleepiness and sleep attacks

Peripheral oedema, ankle swelling, facial oedema
Skin irritation/rash – Rotigotine (10%)

Impulse control disorders
- higher propensity than levodopa

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16
Q

Features of impulse control disorders

A
  • Pathological gambling (more in males)
  • Hypersexuality
  • Compulsive (binge) eating
  • Compulsive shopping (more in females)
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17
Q

Punding

A

stereotyped repetitive behaviours

Often associated with marked dyskinesias and off-state dysphoria and with over-use of levodopa

compulsive performance of repetitive, mechanical tasks, such as assembling and disassembling, collecting, or sorting household objects

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18
Q

Punding

A

stereotyped repetitive behaviours

Often associated with marked dyskinesias and off-state dysphoria and with over-use of levodopa

compulsive performance of repetitive, mechanical tasks, such as assembling and disassembling, collecting, or sorting household objects

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19
Q

MAO inhibitor examples in PD

A
  1. Selegiline
  2. Rasagiline
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20
Q

Good/ Bad aspects of each PD drug class in early PD

A

Levodopa
- well tolerated and most effective/potent
- Increased short-term dyskinesia rate with levodopa but no difference long-term

Dopamine agonists
– medium potency, less well tolerated, less dyskinesia

MAOI-B’s
- very well tolerated, low potency, low dyskinesia

21
Q

Timing of dyskinesias with levodopa

A

Peak dose
* 30-60 min post Ldopa
* Chorea
* entire body/upper half
* Often not aware

End of dose
* 3-4 hours post Ldopa or early morning
* Dystonia
* Often foot
* Often painful

22
Q

Management PEAK dose dyskinesia with levodopa

A
  • reduce levodopa dose size
  • add amantadine
  • add dopamine agonist and reduce levodopa
  • stop entacapone
23
Q

Management END of dose dyskinesia with levodopa

A
  • add entacapone or selegiline
  • decrease dose interval
  • increase levodopa dose size
  • add amantadine
  • add dopamine agonist
23
Q

Amantadine and dyskinesias

A
  • 24% reduction in dyskinesias
  • improved “off” motor performance
  • no change in “on” performance
24
Q

Skin change with amantadine

A

Levido reticularis

harmless but relatively common

25
Q

COMT inhibitors for PD

A

Tolcapone
– Regular LFT testing mandatory
– Scripts have to be written by specialist

Entacapone (Comtan)

26
Q

Amantadine MOA

A

NMDA glutamate receptor antagonist

weak anticholinergic, and љ dopamine release

27
Q

AE amantadine

A

insomnia, livedo

reticularis, confusion, leg oedema, blurred vision

28
Q

Anti-cholinergics in PD

A

all specific anti-muscarinic

benztropine,
procyclidine,
benzhexol

29
Q

AE Anti-cholinergics in PD

A

esp. dry mouth and cognitive impairment also, blurred vision, urinary retention

?? promotes amyloid plaque deposition
? risk factor for dementia

30
Q

RBD treatment

A
  1. Clonazepam
  2. Melatonin
    - increases REM sleep atonia levels
    - useful in those with comorbid OSA or dementia.
31
Q

Incidence of Parkinson’s dementia in PD

A

~ 10% per year

32
Q

Dementia in PD - treatment

A
  • cholinesterase inhibitors
    – rivastigmine
    – donepezil
    – no evidence for benefit in PD-MCI
  • memantine
  • no convincing evidence (yet) for cognitive training or physical exercise or diet, hearing aids
33
Q

Treatment of Psychosis in Parkinson’s

A

Hallucinations
– benign hallucinations of presence are common (don’t treat)
– usually visual, but can be tactile, auditory (treat unless rare)

  • Paranoid psychosis – must be treated urgently!

Step wise progression of management
1. quetiapine
2. reduce PD drugs one by one, starting with the least potent; levodopa should be maintained
3. cholinesterase inhibitors (donepezil) if dementia/confusion
4. clozapine if ongoing psychosis

34
Q

DBS location and effects

A
  • Thalamic surgery (historically done)
    – good mainly for tremor
  • Deeper - Pallidal, subthalamic surgeries have more global effect
35
Q

Selection criteria fo DBS in PD

A

–Typical PD
will never be better than. their best L.dopa response

–Medically healthy

–No dementia

–No psychosis or severe hallucinations

–<70 yrs

36
Q

RED Flags in movement disorder (For not Parkinson’s disease)

A
  • No tremor
  • symmetric signs
  • early falls (in the first year)
  • dysphagia or marked speech problems
  • urinary incontinence
  • early dementia
37
Q

Subforms of MSA

A

MSA-C: cerebellar predominant form
– nystagmus, dysarthria, ataxia

  • MSA-: parkinsonism predominant form
    – mainly akinetic-rigid (symmetric rigidity, little tremor, poor postural reflexes).
38
Q

Main clues for MSA-P

A
  • erectile failure (Men)
  • urinary incontinence (Women)
  • postural hypotension

Other
* not much tremor
* early instability
* pyramidal/cerebellar signs
* poor response to levodopa
* more rapid progression

39
Q

Pathophys MSA

A

Alphasynucleinopathy

40
Q

antecollis

A

Flexed neck

41
Q

MSA on MRI

A

HOT cross bun sign
- in the pons

Putaminal ring sign
- quite specific

42
Q

Subtypes of PSP

A

Classic PSP - “Richardson’s syndrome“
* characterised by the classic features of PSP:
– early onset of falls
– supranuclear down gaze palsy (or slow vertical saccades)
– postural instability
– Frontal dementia.

“PSP-Parkinsonism” (PSP-P)
* characterised by:
– asymmetric onset
– tremor
– response to levodopa
– Better prognosis.

43
Q

PSP on MRI

A

Hummingbird sign
- wasting of the midbrain

44
Q

Pathology in CBS

A
  • Commonest pathology is corticobasal degeneration (a tauopathy) but may be due to other pathologies:
    – PSP
    – Pick disease
    – AD
    – DLB
    – Creutzfeld–Jakob disease
45
Q

Commonest presentation of CBS.

Features of CBS

A

a useless rigid jerking arm.

Other features
– asymmetric akinetic-rigid syndrome
– apraxia
– frontal lobe dementia
– ± limb pain/cortical sensory loss
– ± myoclonus
– ± alien limb phenomenon
– ± oculomotor apraxia (delay in launching saccades
– ± supranuclear gaze palsy (not as severe as PSP, often issues intiating)

46
Q

Drugs -> Drug induced PD

A
  • Neuroleptics
  • Antiemetics
  • Lithium
47
Q

Clues for drug induced PD clinically

A
  • Symptoms and signs often symmetric
  • Tremor may be absent
48
Q

Arteriosclerotic Parkinsonism

Clinical presentation

A
  • Superficial appearance of parkinsonism
  • “lower half parkinsonism”
  • expressive face
  • normal arm swing
  • pyramidal signs (hyperreflexia, extensor plantars)
  • rigidity is gegenhalten or spastic
  • tremor – absent or postural

Dunedin RACP Study Course (31 decks)

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