PD lecture Atnc

Parkinson’s diseaseParkinson’s disease

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Essay on the shaking palsyEssay on the shaking palsyJames Parkinson 1817James Parkinson 1817

“involuntary tremulous motion,with lessened muscular power, in part not in action and even when supported ;with a propensity to bend the trunk forward, and to pass from a walking to a running pace , the senses and intellect being uninjured”


PathologyPathologyLoss of pigmented cells in substantia nigra

Intracellular cytoplasmic inclusion bodies ( Lewy bodies )


Parkinson disease is characterised by loss of Dopaminergic cells in the substantia nigra leading to abnormal activity in the basal ganglia as a whole

This leads to

-A decrease in the activity of the direct GABAergic pathway

-An increase in the activity of the indirect GABAergic pathway


Uptake of radio-labelled L-Dopa in striatum of normal compared to PD brain


Clinical FeaturesClinical Features

T

R

A

P

Tremor

Rigidity

Akinesia / Bradykinesia

Postural instability


Micrographia

=manifestation of bradykinesia


Overview of drug treatmentOverview of drug treatment

1. L-Dopa ( bypass rate limiting stem of Dopamine synthesis)

2. Dopamine agonists ( direct effect on striatum )

3. COMT inhibitors ( less peripheral inactivation of L-Dopa )

4. Selegeline ( MAOb) inhibitor ? Neuroprotective

5. Muscarinic antagonists ( act on striatal interneurons)

6. Amantadine ( mechanism unclear ? Dopamine release )


Treatment strategies Treatment strategies

1. The conservative approach

2. The neuroprotective approach

3. The symptomatic approach


Conservative approachConservative approach

1. Avoid all drugs until symptoms are troublesome

2. When symptoms become troublesome start amantadine and an anticholinergic

3. When symptoms become disabling introduce L-Dopa or agonists at minimal doses


Neuroprotective approachNeuroprotective approach

1. All newly diagnosed cases should be started on Selegeline

2. When symptoms become disabling add dopaminergic drugs


Symptomatic approachSymptomatic approach

At diagnosis treatment immediately started with dopaminergic drugs

Treatment continually modified in order to maintain maximum function for the maximum amount of time


Clinical fluctuations in PDClinical fluctuations in PDConditionCondition ManagementManagement

Wearing-off of L-Dopa effectWearing-off of L-Dopa effect Decrease between dose Decrease between dose intervalinterval

Sustained release L-DopaSustained release L-Dopa

Add DA agonistAdd DA agonist

Increase dose Increase dose

Add COMT inhibitorAdd COMT inhibitor

Delayed onset of responseDelayed onset of response Ensure L-Dopa not given with Ensure L-Dopa not given with protein.protein.

Give antacidsGive antacids

“ “ Off ” periodsOff ” periods Increase dose of L-DopaIncrease dose of L-Dopa

Increase dose frequencyIncrease dose frequency

Give before mealsGive before meals

On-Off phenomenonOn-Off phenomenon Very difficult to treatVery difficult to treat

Sustained release Sustained release preparationspreparations


Dyskinesias in PDDyskinesias in PDTypeType ManagementManagement

Peak-dose dyskinesiaPeak-dose dyskinesia Decrease each dose of L-Decrease each dose of L-DopaDopa

Add Dopamine agonistAdd Dopamine agonist

Add amantadineAdd amantadine

MyoclonusMyoclonus ClonazepamClonazepam

Decrease L-DopaDecrease L-Dopa


Psychosis in PDPsychosis in PD

Increased incidence in

- Elderly

- Pre-existing psychiatric conditions

Should only use atypical antipsychotic medications….in particular

CLOZAPINE - needs monitoring of white cell count

QUETIAPINE- no monitoring necessary

- now possibly drug of choice


The EndThe End

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PD lecture Atnc

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