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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
Amantadine and dyskinesias
* 24% reduction in dyskinesias * improved “off” motor performance * no change in “on” performance
24
Skin change with amantadine
Levido reticularis harmless but relatively common
25
COMT inhibitors for PD
Tolcapone – Regular LFT testing mandatory – Scripts have to be written by specialist Entacapone (Comtan)
26
Amantadine MOA
NMDA glutamate receptor antagonist weak anticholinergic, and љ dopamine release
27
AE amantadine
insomnia, livedo reticularis, confusion, leg oedema, blurred vision
28
Anti-cholinergics in PD
all specific anti-muscarinic benztropine, procyclidine, benzhexol
29
AE Anti-cholinergics in PD
esp. dry mouth and cognitive impairment also, blurred vision, urinary retention ?? promotes amyloid plaque deposition ? risk factor for dementia
30
RBD treatment
1. Clonazepam 2. Melatonin - increases REM sleep atonia levels - useful in those with comorbid OSA or dementia.
31
Incidence of Parkinson's dementia in PD
~ 10% per year
32
Dementia in PD - treatment
* 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
Treatment of Psychosis in Parkinson’s
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
DBS location and effects
* Thalamic surgery (historically done) – good mainly for tremor * Deeper - Pallidal, subthalamic surgeries have more global effect
35
Selection criteria fo DBS in PD
–Typical PD will never be better than. their best L.dopa response –Medically healthy –No dementia –No psychosis or severe hallucinations –<70 yrs
36
RED Flags in movement disorder (For not Parkinson's disease)
* No tremor * symmetric signs * early falls (in the first year) * dysphagia or marked speech problems * urinary incontinence * early dementia
37
Subforms of MSA
MSA-C: cerebellar predominant form – nystagmus, dysarthria, ataxia * MSA-: parkinsonism predominant form – mainly akinetic-rigid (symmetric rigidity, little tremor, poor postural reflexes).
38
Main clues for MSA-P
* 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
Pathophys MSA
Alphasynucleinopathy
40
antecollis
Flexed neck
41
MSA on MRI
HOT cross bun sign - in the pons Putaminal ring sign - quite specific
42
Subtypes of PSP
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
PSP on MRI
Hummingbird sign - wasting of the midbrain
44
Pathology in CBS
* Commonest pathology is corticobasal degeneration (a tauopathy) but may be due to other pathologies: – PSP – Pick disease – AD – DLB – Creutzfeld–Jakob disease
45
Commonest presentation of CBS. Features of CBS
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
Drugs -> Drug induced PD
* Neuroleptics * Antiemetics * Lithium
47
Clues for drug induced PD clinically
* Symptoms and signs often symmetric * Tremor may be absent
48
Arteriosclerotic Parkinsonism Clinical presentation
* 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

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