Parkinson's Flashcards

1
Q

What is lost in PD? What is first seen?

A

Substantia nigra pars compacta and DA neurons, olfactory bulb, locus ceruleus (greatest loss), nucleus basalis (Meynert - ACh); fMRI loss in posterior putamen

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2
Q

Where is the locus ceruleus? What and where does it project?

A

Rostral pons PAG, NE to “everywhere”

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3
Q

What are Lewy bodies?

A

Cytoplasmic inclusions of ubiquitin, alpha-synuclein in SNpc, etc. in PD

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4
Q

What types of lesions cause dysdiadochokinesia?

A

Pontocerebellum, basal nuclei

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5
Q

Why does PD cause poverty of eye movements?

A

SNpr not damaged, inhibits SC deep layers, which leads to inhibition of reflexive saccades, also inhibits FEF voluntary saccades.

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6
Q

What are the best predictors of idiopathic PD?

A

Resting tremor, asymmetrical motor presentation, L-dopa responsiveness

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7
Q

What is secondary parkinsonism?

A

Caused by antipsychotic Rx DA blockers, MPTP (heroin contaminant, kills DA neurons)

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8
Q

Why is olfactory deficit important in PD?

A

Required for Dx idiopathic PD, one of earliest deficits in PD and AD, distinguishes from other parkinsonisms

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9
Q

What are neuropsychiatric problems associated with PD?

A

Delirium with anti-PD drugs, depressed, anxiety, demented (dementia with Lewy bodies), cognitive impairment

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10
Q

What are the most common complications with PD?

A

Falls, motor fluctuations, dyskinesias, dementia/depression

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11
Q

Why is L-dopa a treatment option for PD?

A

Can’t use systemic DA because BBB, side effects; tyrosine doesn’t work

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12
Q

What is carbidopa?

A

AADC blocker inhibits L-dopa conversion to dopamine in blood stream until past BBB

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13
Q

What are problems with L-dopa?

A

Neural loss still occurs, may worsen, effectiveness gradually decreases, changes in efficacy for no reason, disabling dyskinesias

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14
Q

Why are DA agonists a good or bad idea?

A

Reduce risk of dyskinesia, may have neuroprotective side effects; hallucinations/psychosis, avoid in elderly or cognitively impaired

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15
Q

What are surgical treatments for medically resistant PD?

A

Unilateral thalatomy for tremor (VIM nuc for various tremors); neural transplant; DBS of STN, VIM, GPi; unilateral pallidotomy for tremor, bradykinesia

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16
Q

What are the inputs to the VA, VL, VIM, and VP?

A

VA: GPi; VL: GPi & cerebellum; VIM: proprioceptive; VP: proprioceptive, somatosensory

17
Q

What is GAD (glutamatic acid decarboxylase)?

A

Gene therapy, converts glutamate to GABA