parkisons Flashcards
what are the classifications of PD
primary/idiopathic
secondary
heredogenerative
multiple-system degeneration or parkinsonism-plus
give examples of primary/idiopathic PD
parkinson’s disease
juvenile parkinsonism
give examples of secondary PD
infections, drugs, toxins, vascular or trauma
toxoplasmosis
- from feces of cats c parasites; common in HIV pts that causes lesion on BG
give examples of heredogenerative PD
huntington’s or wilson disease
give examples of multiple-system degeneration or parkinsonism-plus
progressive supranuclear palsy
corticobasal degeneration
lew body dementia
multisystem atrophy
discuss progressive supranuclear palsy
PSP
- rigidity
- diff c vertical gaze
- has ssx of PD
discuss lewy body dementia
LBD
- combi of parkinsons and dementia
- no cure; often presesnt c depression
discuss multisystem atrophy
striatonigral degeneration - affects striatum and SN
olivopontocerebellar atrophy - OCPA
- bradykinesia
- balance probs
- sporadic or sponty in occurence
shy drager syndrome
- ssx of PD but has autonomic probs; BP or cant sweat
discuss prevalence of PD
20-30 per 100k and more common in males (3:2)
rising prevalence with age
discuss the pathogenesis of PD
neurodegenerative disease c depigmentation of the substantia nigra = loss of dopaminergic input in BG = extrapyramidal sx
from imbalance bet dopamine (inhib) and ACH (excitatory); normal ACH but onti dopamine kaya hyperkinetic - resting tremors
PD is both hypokinetic and hyperkinetic
discuss the etiology of PD
unknown tlaga but
influence of aging - since neurons also degenerate
environmental toxins - aluminum cans
genetics pero saks lng
oxidative stress - seen in DM AND HTN
X-LINKED DYSTONIA - PD
exp oxidative stress theory
alterations of SN in PD is suggestive of oxidative damage
- inc iron, aluminum
- lack of isoferritins
- reduced glutathione
- selective defect in complex 1 of mitochondrial respiratory chain
- damage to lipids, DNA and proteins
- DM and HTN that leads to dementia
in essence what are the possible causes of PD
oxidative stress
mitochondrial dysfunction
abnormal protein clearance
excitotoxicity
protein handling dysfucntion
age for young onset PD
onset < 40 yo
age for juvenile onset PD
onset < 20 yo
what is parkin mutation
major cause of young onset autosomal recessive PD and isolated juvenile PD
this is usually seen in autosomal dominant PD
mutations in the 𝝰 synuclein and ubiquitin carboxyl hydrolase:
most PD symptoms do not appear til striata DA levels decline by ______
at least 70-80%
symptoms of PD
TRAP
- tremors: resting
- rigidity: cogwheel
- akinesia or brady: rebound or slow initiation and execution
- postural instab: imbalance, stoop posture; pwede din gait; shuffling gait c lack of heel strike; righting reflex
further discuss resting tremors
4-6 Hz
will begin in the hand unilaterally and usually at early stage
disappears c voluntary movement but in advanced di na nawawala
disappears with sleep; more present in > 80 yo and if stressed
pill rolling - unconscious movement of index and thumb
basta dapat ma differentiate with essential (8 Hz) and physiological (12Hz) which are more of cerebellar problem
further discuss limb rigidity
inc tone and resistance to movement of both UE and LE
should be cogwheel and differentiated from spastic
ratchet like resistance dapat not matigas then mag give in which is spastic
further discuss akinesia or bradykinesia
dec speed & amplitude of complex voluntary movement
slowness in initiating and sustaining movement
how to elicit:
- micrographia: lumiliit sulat
- tapping fingers
- twiddling of hands
- pinching and circling
- tapping c heel
usually one side is slower in early stages; misdiagnosed as stroke
akinesia is for late stage
further discuss postural instab
how to elicit
- ask pt to stand parang romberg tas usually wide based
- pt will fall is positive test
- off balanced when turning
- parkinsonian gait
- stoop posture
discuss diagnosis for PD from ward and gibb
presence of at least 2/4 cardinal signs; but 2/3 lng at their time since wala pa postural instab
presence of 2 of the ff
- marked response to levodopa
- assym of signs; unilateral
- assymetry at onset
evidence of disease progression
absence of clinical features of alternative dx
absence of etiology known to cause similar features; secondary PD
stage 0 PD
no clinical signs or evidence
stage 1 PD
Unilateral involvement
major features of tremor, rigidity or bradykinesia
minimal functional impairment
stage 2 PD
bilateral involvement but no postural abnormalities
stage 3 PD
mild to mod bilateral disease; mild postural imbalance
but can still function indep
stage 4 PD
bilateral involvement c postural instab and requires assistance
stage 5 PD
severe; pt is restricted to bed or w/c unless aided
