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– 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 dopamine-producing 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

• 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

• 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

• Oxidative stress• Mitochondrial dysfu• Excitotoxicity• abnorma

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

Pathology

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

Pathophysiology

• Degeneration of substantia nigra• Reduced production of dopamine

Clinical Manifestations

• Bradykinesia – bumabagal• Tremor• Rigidity *Stooped posture

Symptoms

• T- Tremors at rest• R- Rigidity• A- Akinesia/Bradykinesia • P- Postural instability

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

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

• Stooped, nanginginig ang kamay• Shuffling gait • Righting reflex• equilibrium