1. Parkinson’s Disease
superKAT :)

2. Parkinsonism Neurological syndrome Combination of: 77% PD
Rest tremors
Rigidity
Bradykinesia
77% PD
12% Parkinson plus syndromes
5% Drug induced Parkinsonism
*not recognized early

3. Primary/idiopathic parkinsonism
Parkinson’s disease
Juvenille parkinsonism
Secondary
Infectious, drugs, toxins, vascular, trauma
Heredodgenerative parkinsonism
Huntington’s
Wilson
Multiple-system degeneration/ parkinsonism-plus
CBD
LBD
Multisystem atrophy
PSP

4. Definition – Parkinson’s
Described by James Parkinson in 1817 as the “shaking palsy”
Chronic progressive disorder occurring in the Central Nervous System
Results from degeneration of dopamine-producing cells in the susbtantia nigra (pars compacta – degenerate more and pars reticularis)

5. 2nd most common neurodegenerative disease after Alzheimer’s disease
Age-related, progressive disorder
Dopamine, critical modulator of striatal output, is markedly decreased PD = control fine skillful movements

6. Prevalence PD is estimated to affect 100-180 in 100,000
Annual incidence of 4-20 per 100,000
Rising prevalence with age
Male: Female ratio is 3:2

7. Pathogenesis Neurogenerative
Loss of dopaminergic input to basal ganglia (extrapyramidyal system)
Result in imbalance with dopamine and acetylcholine

8. Etiology Unknown Oxidative stress Proposed etiology Aging
Environmental toxins
Genetic susceptibility

9. Oxidative stress theory
Increased iron level
Lack of compensatory rise in isoferritins
Increased aluminum levels
Reduced glutathione levels
Selective defect in complex I of mitochondrial respiratory chain
Evidence of oxidative damage to
Lipids, DNA, proteins, tyrosine-containing molecules

10. Oxidative stress
Mitochondrial dysfu
Excitotoxicity
abnorma

11. genetics Young onset <40yrs Juvenile onset <20yrs
Parkin mutations: parkin gene
Mutations in the alpha synuclein and ubiquitin carboxy hydrolase: seen in autosomal dominant PD

12. Pathology
Loss of dopaminergic (DA) cells located in susbtantia nigra: most symptoms do not appear striata DA levels decline by at least 70-80%

13. Pathophysiology Degeneration of substantia nigra
Reduced production of dopamine

14. Clinical Manifestations
Bradykinesia – bumabagal
Tremor
Rigidity
*Stooped posture

15. Symptoms T- Tremors at rest R- Rigidity A- Akinesia/Bradykinesia
P- Postural instability

16. Tremors 4-6Hz Resting Disappears with voluntary movement
Disappears with sleep
Accentuated by stress/anxiety
Pill rolling
*Essential tremor & Physiology tremors 8-12 Hz and are kinetic and/or postural

17. Limb rigidity Resistance to passive movements of limbs
Involuntary hypertonia
Cogwheel

18. Bradykenisa
Decreased speed and amplitude of complex voluntary movements
Slowness and initiating and sustaining movement
Fragmented
Micrographia – lack of movement of the arm/difficulty
Tapping fingers
Twiddling

19. Postural instability Stooped, nanginginig ang kamay Shuffling gait
Righting reflex
equilibrium