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PARKINSON’S DISEASE
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Page 1: Parkinson's disease and alzheimer's disease

PARKINSON’S DISEASE

Page 2: Parkinson's disease and alzheimer's disease

INTRODUCTION

Parkinson’s disease is a chronic

neurodegenerative movement disorder affecting

voluntary and emotional movements and most

commonly seen in the elderly, but is also found

in the young and inexorably progresses leading

to significant disability.

Page 3: Parkinson's disease and alzheimer's disease

EPIDEMIOLOGY

Primarily a disease of the elderly

Mean age 55, Range 20 - 80 years

Juvenile parkinsonism- Less than 20 years

M/F = 3:2

Prevalence increases with age

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PATHOPHYSIOLOGY

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Tremors Rigidity BradykinesiaPostural

instabilityDementia Sialorrhoea

SYMPTOMS

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Tremors – hands and head develop involuntary movements when at rest; pin-rolling sign (finger and thumb)

Muscle rigidity – arthritis-like stiffness, difficulty in bending or moving limbs; poker face

Brandykinesia – problems chewing, swallowing or speaking; difficulty in initiating movements and controlling fine movements; walking becomes difficult.

Postural instability – humped over appearance, prone to falls

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Chemical Balance in Corpus Striatum

Excitatory

Cholinergic

pathway

Inhibitory

Dopaminergic

pathway

BALANCE

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Chemical Balance in Corpus Striatum

Excitatory Cholinergic

pathway

Inhibitory

Dopaminergic

pathway

Imbalance

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Parkinson’s disease - Pathophysiology

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CAUSES

Unclear, but is a number of factors:

– Environmental – toxins

– Free Radicals – there is a increase in post-

mortem brain sections

– Aging – age related decline in dopamine

production

– Genetic – possible, no single gene identified

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TREATMENT

The Drugs:

– Dopaminergic drugs (improving dopamine

functioning)

• Levodopa

• Dopamine receptor agonists

• Amantadine

• Selective monoamine oxidase B inhibitors

• Catechol-O-methyltransferase inhibitors

– Antimuscarinic drugs (Ach inhibitors)

Page 12: Parkinson's disease and alzheimer's disease

Levodopa (Madopar & Sinemet)

Can not administer dopamine directly, as it does

not cross the blood brain barrier

A natural amino acid that the brain converts into

dopamine (replacement therapy) used since the

1960’s

To make it slow release, combined with

benserazide (an enzyme inhibitor) to create co-

beneldopa or co-careldopa (Sinemet)

Dose = 50, 100 or 200mg (12.5, 25 or 50mg)

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Surgical treatment

Deep brain stimulation

Pallidotomy

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ALZHEIMER’S DISEASE

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Although the risk of developing AD increases with age – in most

people with AD, symptoms first appear after age 60 – AD is not a part

of normal aging.

Alzheimer’s disease is an neurodegenerative,

irreversible, progressive brain disease that

slowly destroys memory and thinking skills.

What is Alzheimer’s disease (AD) ?

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PATHOLOGY

The main pathological feature of AD comprise;

Deposition of β Amyloid protein(Aβ) in selective areasof brain like cortex , hippocampus , Amygdala .

Intraneuronal neurofibriliary tangles which comprisesof the aggregates of highly phosphorylated form ofnormal neuronal protein (Tau).

Marked decrease in choline acetytranferase and loss ofcholinergic neuron in brain.

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video

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CURRENT TREATMENT

03/01/2014

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Class Drug

Nootropics Piracetam

Metabolic Enhancer Nicergoline

Cholinergic activators Tacrine

Vasoactive central protector Pyritinol