Transcript Parkinson`s Disease

Parkinson’s Disease
superKAT :)
Parkinsonism
• Neurological syndrome
• Combination of:
– Rest tremors
– Rigidity
– Bradykinesia
• 77% PD
• 12% Parkinson plus syndromes
• 5% Drug induced Parkinsonism
*not recognized early
• Primary/idiopathic parkinsonism
– Parkinson’s disease
– Juvenille parkinsonism
• Secondary
– Infectious, drugs, toxins, vascular, trauma
• Heredodgenerative parkinsonism
– Huntington’s
– Wilson
• Multiple-system degeneration/ parkinsonism-plus
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CBD
LBD
Multisystem atrophy
PSP
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 dopamineproducing cells in the susbtantia nigra (pars
compacta – degenerate more and pars
reticularis)
• 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
Prevalence
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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
Pathogenesis
• Neurogenerative
• Loss of dopaminergic input to basal ganglia
(extrapyramidyal system)
• Result in imbalance with dopamine and
acetylcholine
Etiology
• Unknown
• Oxidative stress
• Proposed etiology
– Aging
– Environmental toxins
– Genetic susceptibility
Oxidative stress theory
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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
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Oxidative stress
Mitochondrial dysfu
Excitotoxicity
abnorma
genetics
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Young onset <40yrs
Juvenile onset <20yrs
Parkin mutations: parkin gene
Mutations in the alpha synuclein and ubiquitin
carboxy hydrolase: seen in autosomal
dominant PD
Pathology
• Loss of dopaminergic (DA) cells located in
susbtantia nigra: most symptoms do not
appear striata DA levels decline by at least 7080%
Pathophysiology
• Degeneration of substantia nigra
• Reduced production of dopamine
Clinical Manifestations
• Bradykinesia – bumabagal
• Tremor
• Rigidity
*Stooped posture
Symptoms
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T- Tremors at rest
R- Rigidity
A- Akinesia/Bradykinesia
P- Postural instability
Tremors
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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
Limb rigidity
• Resistance to passive movements of limbs
• Involuntary hypertonia
• Cogwheel
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
Postural instability
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Stooped, nanginginig ang kamay
Shuffling gait
Righting reflex
equilibrium