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Brain And Behaviour > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Symptoms of PD?

A 
Bradykinesia
Resting tremor
Rigidity (cogwheel/lead pipe)
Sleep disturbances (flailing out)
Excessive salivation
Shuffling gait
Falls
Freezing of gate
Masked faces
Impaired swallowing 
Anosmia
Micrographics
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2
Q

Risk factors?

A

Family history
Smoking
pesticide exposure
Age (17.4 per 100,000 person years between 50 and 59 increases to 93 per 100,000 person years between 70-79)

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3
Q

What compensatory changes mean PD only manifests when a significant proportion of neurons have been lost in the nigrostiatal pathway?

A

Increase in TH activity

Increase in postsynaptic dopamine receptors in the striatum

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4
Q

What other dopaminergic pathway may degenerate in PD?

A

Those from the VTA (mesolimbic may degenerate up to 50%)

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5
Q

What other neurons may degenerate other than dopaminergic ones?

A

Noradrenergic (locus coeruleus)
Cholinergic (basal forebrain)

These may be responsible for the non motor symptoms of PD

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6
Q

What are the cognitive dysfunctions in PD?

A

Mood disturbances
Cognitive defects
Dementia

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7
Q

What mood disturbances are seen in PD?

A

Depression (increases risk of developing dementia)
May be organic or reactionary

Could be due to morphological changes in NA and 5-HT pathways in locus coeruleus and dorsal rap he nucleus

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8
Q

What are the cognitive defects seen in PD?

A

Degeneration of the mesolimbic pathway

Disturbed processes under frontal lobe control

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9
Q

What factors in PD increase th risk of developing dementia in PD?

A

Depression
Prominent gait and speech disordered
Poor L-dopa response

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10
Q

What dementias may be associated with PD?

A

Lewy body dementia

Alzheimer’s (degeneration of the basal nucleus of meynert)

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11
Q

What is psychosis?

A

The inability to distinguish between the subjective experience and external reality

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12
Q

How many PD patients develop psychoso due to l-dopa treatment?

A

20-30%

Those with preexisting cognitive defects are at increased risk

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13
Q

How do you treat PD psychosis without making the PD worse?

A

Reassess patients medication
Pimavanserin (selective serotonin inverse agonist)
Quitiapine

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14
Q

What are Lewy bodies?

A

The hallmark of PD
Insoluble aggregates of alpha Synuclein
Which stain heavily for eosin

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15
Q

Wha factor determines LB morphology

A

The neuroanatomical location

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16
Q

Where else can LB be found?

A

DwLB
multiple system atrophy
Incidental LB pathology (patient who do not have PD…will they have gone on to develop PD?)

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17
Q

What did Braak et al suggest?

A

LB disseminates throughout the brain affecting specific neuroanatomical areas in various stages. Not all PD cases show this progression though

18
Q

What is hypothesised to be the toxic species of PD?

A

Alpha Synuclein oligomers

19
Q

What might LB do?

A

May have a neuroprotective role acting as an aggresome for misfolded proteins which causes neurodegenration

20
Q

What are the aetiologcal theories of PD?

A 
Familial (hereditary)
Viral
Pesticides and chemicals
MPTP (MPP+)
Industrial exposure
21
Q

What genes are associated with monogentic variants of PD

A 
SNCA
LRRK
DJ-1
PARKIN
PINK1
22
Q

How may SNPs are associated with PD

A

~28 (over 20)

Found via genome wide association studies

23
Q

What viral aetiology is associated with a parkinsonian like syndrome?

A

Encephalitis lethargia

24
Q

Why is MPTP useful?

A

Provides a animal model for PD as is selective for mono amino neurons, particularly those in the SN

25
Q

What industrial chemicals cause degeneration of striatum and its outputs producing a PD like syndrome?

A

Manganese

Carbon disulphide

26
Q

Ultimately, do we know what causes Parkinson’s disease?

A

No.
However RNAi studies have indicated that several genes involve din protein trafficking are genetic modifiers for this disease e.g. The RabGTPases

27
Q

How can we treat PD with medications?

A 
Dopamine therapy (give L-DOPA as dopamine cannot cross BBB) + carbidopa
Dopamine agonists
MAO-B inhibitors
COMT inhibitor
Anticholingerics
Amantidine
28
Q

What are the problems with L-Dopa?

A

ADRS (psychosis, dyskinesia, N+V, hypotension)
Effect decrease overtime
Deietary considerations
?neurotoxic

29
Q

What are the different types of dopamine agonists? Give an example

A

Ergot derived - Bromocryptine
Non ergot - ropinirole
Subcutaneous - apomorphine

30
Q

What are the disadvantages of dopamine agonists?

A

Increased risk of psychosis
Less efficacious than L-Dopa
Impulse control disordered i.e. Pathological gambling

31
Q

name a MAO-B inhibitor

A

Selegiline

32
Q

How do MAO-B inhibitors work?

A

Bloc dopamine break down in DOPAC

Can be used alone or in combination with LDopa to prolong its effects

33
Q

name come COMT inhibitors

A 
Tolcapone
Entacapone (does not cross BBB)
34
Q

How does entacapone work?

A

Breaks peripheral break down of Ldopa to a compound which competes with it for entry into the CNS
Thus needs to be even with L-Dopa
Prolongs L dopa effects and helps eliminate wearing off

35
Q

What is procyclidine useful for?

A

Anticholingeric good for treating tremor

36
Q

What does Amantadine do?

A

Increases dopamine release
?inhibits uptake

Unclear mechanism

37
Q

where can graft to treat PD come from?

A

Stem cells and the adrenal medulla

38
Q

What do grads from the adrenal medulla show?

A

Variable results and graft do not survive well

39
Q

What do graft from foetal stem cells show?

A

Short lived improvements

May accumulate alpha Synuclein themselves over time

40
Q

What surgical interventions are there for PD?

A

Lesions (thalamus, STN, globus pallidus)

Deep brain stimulation (electrodes often placed in subthalamic nucleus to cause depolarisation block of Gpi)

Brain And Behaviour (12 decks)

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