Parkinson's Disease Flashcards

1
Q

What is the pathophysiological and macroscopical aspect of parkinsons disease?

A

loss of pigmented dopamine neurons in striatum, because no input from subst. nigra&raquo_space; less inhibition of GPi, making it overreactive&raquo_space;increased inhibtion of thamalus&raquo_space; hypokinesia

decreased pigmentation on substantia nigra and locus ceruleus
lewy bodies: abnormal aggragation of proteins

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2
Q

Which mechanisms lead to neuronal loss in PD?

A
oxidative stress
mitochondrial dysfunction
excitotoxicity
glial cell activation
apoptosis
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3
Q

What is parkinsons disease?

A

progressive, multifocal neurodegenerative disease

  • dopaminergic/non dopaminergic
  • CNS/ PNS affected
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4
Q

How is the progression of the lewy inclusion bodies?

A

typical pregression from: medulla&raquo_space; pons&raquo_space; midbrain&raquo_space; mesocortex&raquo_space; neocortex

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5
Q

Etiology of parkinson disease

A

genes, toxins, endogenous, trauma

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6
Q

Epidemiology of parkinson disease

A

onset: 40 - 70 yea, peak in 6th decade

M>F

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7
Q

What are the early signs of parkinson disease

A
  • stiffness
  • pain and paresthesia of limb
  • constipation
  • sleeplessness
  • decr. voice volume

others: decr. fine motor skills and sense of smell, loss of appetite, tremor with anxiety

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8
Q

Clinical subtypes of parkinson disease

A
  • young age and slow progression
  • old age and fast progression
  • tremor dominant
  • postural instability and gait difficulty
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9
Q

How is the posture of a patient in parkinson disease

A

flexed posture, less of reflexes, no balance, festination, freezing phenomenon

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10
Q

What are the clinical signs of dementia with lewy bodies

A
  • fluctuating attention and alertness episodes
  • halluzinations
  • parkinsonian motor features
  • early extrapyr. features (in alzheimer they are late)
  • less prominent anterograde memory loss (in alzheimer is prominent)
  • executive function deficits
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11
Q

How to differentiate between dementia with lewy bodies and parkinson disease?

A

parkinson: parkinsonian signs are present more than 12 month before cognitive impairment

DLB: parkinsonian signs are seen less than 12 month before cognitive impairment

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12
Q

Treatment of parkinsons disease

A

dopaminergic agents:

  • levodopa
  • dopamine agonists (ergot and non-ergot)
  • selective MAO-B inhibitors

non dopamin. agents:

  • anticholinergic agents
  • n-methyl-di-aspartate antagonist
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13
Q

describe pyramidal spasticity and parkinsonian rigidity

A

spasticity:
lesion in corticospinal pathway, unidirectional, passive movement speed dependent, UMN lesion
claspknife phenomenon: initial rigidity during passive movement, at sharp angel resistance disappears suddenly

rigidity:
extrapyramidal lesion, referred to lesion in basal ganglia, bidirectional, not speed dependent, rigidity present during whole passive movement,
leadpipe rigidity: rigidity from beginning to end of movement
cogwheel rigidity: rigidity with interposed tremor signs (parkinon feature)
plasticity: newly places limb stays in that position

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14
Q

features of parkinson tremor

A

typical rest tremor, 4 - 6 Hz
most prominent at distal part of extremity
pill rolling tremor
exacerbated during provocation

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15
Q

features of progressive supranuclear palsy

A
supranuclear ophtalmoplegia
pseudobulbar palsy
prominent neck dystonia
parkinsonism
impaired postural reflexes
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16
Q

which motor sign is necessary for the positive diagnosis of parkinson

A

bradykinesia

additional: rigidity, 4-6 Hz tremor, postural instability with exclusion on any other possible cause

17
Q

drug of choice for psychosis in parkinsonism?

A

levodopa

18
Q

what are the sideeffects of levodopa treatment?

A
  • short HL causes motor and nonmotor fluctuations (gait and postural difficulties, depression, dementia)
  • dyskinesia
  • neurological problems: hallizin., behavioral disorders
  • daytime sleepiness
19
Q

which are the motor fluctuations in parkinson?

A

gait difficulties
postural imbalance
dysarthria

due to short HL, pulsatile dopaminergic stimulation and changes in postsynaptic receptors
reduces sythesis, storage and release of dopamine