Parkinson's Disease Flashcards
What is the pathophysiological and macroscopical aspect of parkinsons disease?
loss of pigmented dopamine neurons in striatum, because no input from subst. nigra»_space; less inhibition of GPi, making it overreactive»_space;increased inhibtion of thamalus»_space; hypokinesia
decreased pigmentation on substantia nigra and locus ceruleus
lewy bodies: abnormal aggragation of proteins
Which mechanisms lead to neuronal loss in PD?
oxidative stress mitochondrial dysfunction excitotoxicity glial cell activation apoptosis
What is parkinsons disease?
progressive, multifocal neurodegenerative disease
- dopaminergic/non dopaminergic
- CNS/ PNS affected
How is the progression of the lewy inclusion bodies?
typical pregression from: medulla»_space; pons»_space; midbrain»_space; mesocortex»_space; neocortex
Etiology of parkinson disease
genes, toxins, endogenous, trauma
Epidemiology of parkinson disease
onset: 40 - 70 yea, peak in 6th decade
M>F
What are the early signs of parkinson disease
- 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
Clinical subtypes of parkinson disease
- young age and slow progression
- old age and fast progression
- tremor dominant
- postural instability and gait difficulty
How is the posture of a patient in parkinson disease
flexed posture, less of reflexes, no balance, festination, freezing phenomenon
What are the clinical signs of dementia with lewy bodies
- 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
How to differentiate between dementia with lewy bodies and parkinson disease?
parkinson: parkinsonian signs are present more than 12 month before cognitive impairment
DLB: parkinsonian signs are seen less than 12 month before cognitive impairment
Treatment of parkinsons disease
dopaminergic agents:
- levodopa
- dopamine agonists (ergot and non-ergot)
- selective MAO-B inhibitors
non dopamin. agents:
- anticholinergic agents
- n-methyl-di-aspartate antagonist
describe pyramidal spasticity and parkinsonian rigidity
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
features of parkinson tremor
typical rest tremor, 4 - 6 Hz
most prominent at distal part of extremity
pill rolling tremor
exacerbated during provocation
features of progressive supranuclear palsy
supranuclear ophtalmoplegia pseudobulbar palsy prominent neck dystonia parkinsonism impaired postural reflexes
which motor sign is necessary for the positive diagnosis of parkinson
bradykinesia
additional: rigidity, 4-6 Hz tremor, postural instability with exclusion on any other possible cause
drug of choice for psychosis in parkinsonism?
levodopa
what are the sideeffects of levodopa treatment?
- short HL causes motor and nonmotor fluctuations (gait and postural difficulties, depression, dementia)
- dyskinesia
- neurological problems: hallizin., behavioral disorders
- daytime sleepiness
which are the motor fluctuations in parkinson?
gait difficulties
postural imbalance
dysarthria
due to short HL, pulsatile dopaminergic stimulation and changes in postsynaptic receptors
reduces sythesis, storage and release of dopamine
