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PBL SEM 3 > 7 - parkinson’s disease : pathophysiolgy and clincal management > Flashcards

7 - parkinson’s disease : pathophysiolgy and clincal management Flashcards

1
Q

age of onset in PD?

A
  • usually >60
  • young onset in 5% - <40
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2
Q

what are the core clinical features of PD?

A
  • bradykinesia, rigidity
  • resting tremor (can also be postural)
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3
Q

describe movement in bradykinesia

A

slow and reduced amplitude

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4
Q

how is rigidity different from spasticity?

A

not velocity dependent, unlike spasticity

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5
Q

what are and what is the main component of Lewy bodies?

A
  • occlusion bodies in neurones
  • a-synuclein = main component — damages neurones, causes degeneration
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6
Q

parkinson’s disease pathology

A
  • Lewy bodies — mainly in substantia nigra
  • degeneration of SNc — loss of dopamine
  • caudo-rostral spread of lewy bodies through brain regions via vagus nerve (starts in brainstem, medulla, olfactory bulb)
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7
Q

genetics in PD?

A
  • monogenic
  • recessive is more common in young onset eg. parkin
  • dominant eg. SNCA, LRRK2
  • dysfunction in number of cellular pathways
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8
Q

environmental factors in PD?

A
  • toxins eg. MPTP (neurotoxin which causes DA degeneration), paraquat (pesticide)
  • possibility of spread of toxic/infective agents from gut/olfactory system
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9
Q

how is PD diagnosed?

A
  1. bradykinesia + tremor and/or rigidity
  2. absence of red flags + at least one of:
  • clear response to dopaminergic therapy
  • levodopa-induced dyskinesia
  • rest tremor
  • olfactory loss (often occurs early on)
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10
Q

what are red flags for idiopathic PD diagnosis?

A
  • absent tremor, symmetrical onset (usually asymmetrical in PD)
  • early gait abnormality and falls (falls usually happen later on in PD)
  • pyramidal tract signs
  • poor levodopa response
  • supranuclear gaze palsy (problem looking up and down)
  • dysautonomia, ataxia stridor (multiple system atrophy)
  • apraxia, myoclonus, alien limb
  • early dementia
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11
Q

what are some non-motor features of PD?

A
  • cognitive impairment eg. dementia, behavioural problems
  • visual hallucinations
  • mood disorders
  • olfactory deficit
  • pain (brainstem nuclei involved?)
  • sleep disorders
  • mood disorders
  • orthostasis
  • constipation, urine and erectile dysfunction
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12
Q

what are possible pre-motor features?

A
  • REM sleep behaviour disorder (people act out their dreams)
  • anosmia
  • constipation
  • depression
  • pain
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13
Q

how do symptoms of PD develop throughout the disease?

A
  • starts with autonomic and olfactory disturbances
  • sleep and motor disturbances
  • emotional and cognitive disturbances (spread of Lewy bodies to cortex)
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14
Q

what are enkephalin and dynorphin substance P like in PD?

A
  • increased ENK due to overactive indirect pathway
  • decreased dynorphin due to decrease in direct pathway
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15
Q

why is there decreased movement in PD?

A

more inhibiton of thalamus

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16
Q

why do you get bradykinesia?

A
  • increased inhibitory output to central pattern generators in brainstem
  • increased inhibitory output to thalamus and motor cortex
  • abnormal B band oscillations (20 Hz) in basal ganglia circuit
17
Q

what happens to oscillations in treatment?

A

‘off’ — more oscillations
on treatment — oscillations normal

18
Q

what does amantadine do?

A

blocks glutamatergic NMDAR in basal ganglia

19
Q

what is and what causes rigidity?

A
  • increase in muscle tone
  • more obvious during slow movements (unlike spasticity)
  • peripheral — reduced inhibiton from type Ib fibres, overactive type II fibres, increased activity due to peripheral stimulation
  • central — altered activity in GABA and ACh interneurons, altered inhibition in indirect pathway, increased responsiveness of STN/GPi firing to peripheral stimulation
20
Q

describe tremor in PD

A
  • absent in around of 30% patients
  • less response to dopaminergic drugs
  • not just basal ganglia output
  • generated at level of thalamo-cortical-cerebellar loops (modified by basal ganglia activity)
  • non-dopaminergic pathways eg. 5-HT?
21
Q

what is the gold standard treatment of PD?

A

L-DOPA

22
Q

name 2 COMT inhibitors

A

entacapone, tolcapone

23
Q

L-DOPA vs DA?

A
  • L-DOPA is the precursor to DA — converted to DA once crossed BBB
  • DA broken down by dopamine decarboxylase in periphery
  • L-DOPA can cross BBB
24
Q

what must levadopa be prescribed with?

A

a DA decarboxylase inhibitor to prevent periphery breakdown

25
Q

levodopa vs dopamine agonists

A

levodopa
- better motor improvement in short term
- reduced freezing of gait
- more dyskinesia, possibly in long term

dopamine agonists
- less dyskinesia and linger latency to dyskinesia
- more adverse effects such as nausea, postural hypotension, somnolence
- impulse control disorders
- withdrawal problems

26
Q

describe motor complications in PD

A
  • wearing off and motor fluctuations
  • L-dopa induced dyskinesia
  • occur in 50% after 4-6 years treatment
  • related to how long you have had the disease
  • young age, disease severity associated
  • genetic factors
  • decreased duration of action and more dyskinesia as disease progresses
27
Q

pathophysiology of motor complications

A
  • brain less able to handle L-DOPA as disease goes on
  • overactive direct pathway
  • underactive indirect pathway
  • too little inhibition and too much excitation — more involuntary movement
28
Q

what are mechanisms of motor complications?

A
  • pulsatile dopaminergic stimulation
  • abnormal handing of dopamine by 5-HT neurones (due to death of DA neurones)
  • abnormal synaptic plasticity
29
Q

how can dyskinesias be treated?

A
  • amantadine — NMDA receptor antagonist, blocks glutamate — reduces dyskinesia by around 40%
  • continuous dopaminergic stimulation — apomorphine (DA agonist by iv) and duodopa (into intestine)
    — fewer fluctuations
30
Q

name some impulse control disorders seen in PD

A
  • pathological gambling
  • hypersexuality
  • compulsive shopping
  • binge eating
31
Q

what are risk factors for impulse control disorders?

A
  • dopamine agonist use > high dose levodopa
  • smoking
  • male
  • young onset PD
  • depression
  • novelty-seeking behaviour
  • family history gambling, alcoholism
32
Q

what can abrupt withdrawal of medications lead to?

A

neuroleptic malignant syndrome — rigidity, muscle breakdown

33
Q

what % of patients are eligible for DBS?

A

10%

34
Q

describe SPECT

A
  • single photons registered by rotating gamma camera
  • low cost, poor resolution
  • long tracer half life
  • widely used
35
Q

describe PET

A
  • 2 y-rays emitted at 180 degrees detected by static ring of detectors
  • higher cost
  • better resolution
  • not available in all hospitals
  • shorter half life
36
Q

what is 18F-fluorodopa in PET bind to?

A

vesicles in brain containing DA

37
Q

what is DA loss like in PD?

A

asymmetric

PBL SEM 3 (49 decks)

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