Presented by

Jessica Faye Manansala

Parkinson's Disease

Is a slowly progressing neurologic movement disorder that eventually leads to disability.

Symptoms 1st appear in 50th decade of lifeParkinson’s disease may be diagnosed at the

aged of 30PD is the 4th most common neurodegenerative

disease.It affects men more frequently than women.

Most cause was unknown

Parkinson's Disease

GeneticAtheriosclerosisHead traumaChronic antipsychotic medsExcessive accumulation of O2Viral infectionAnd some environmental exposure

Factors

Pathophysiology

THREE CARDINAL SIGNS1. Tremor2. Rigidity3. Bradykinesia (abnormally slow movement)Other signs Hypokinesia Gait disturbances Postural instability

Clinical Manifestation

Tremor – rhythmic , slow turning motion of the forearm & hand and a motion of the thumb against the finger as if a rolling pill.

- Present while the pt. is at rest- Tremor increase when the pt. is walking,

concentrating or feeling anxious.Rigidity – resistance to passive limb

movement “cogwheeling” passive movement- Stiffness of the neck, trunk & shoulder is

common.- The pt. may complain shoulder pain (early

signs).Bradykinesia - abnormally slow movementHypokinesia (abnormally diminished

movement) – common appear after tremor

Micrographia – shrinking, slow hand writingDysphonia – soft, slurred, low pitched, and less

audible speech.Shuffling gait – the pt. may walk faster and

faster, trying to move the feet forward under the body’s center of gravity.

Other manifestationsExcessive & uncontrolled sweatingProxysmal flushingGastric & urinary retentionOrthhostatic hypothensionConstipationDementiaDepression

PET (Positron emission tomography)scanning – used in evaluating levodopa (precursor of dopamine) uptake and conversion to dopamine.

Patients historyPresence of 2 or 3 cardinal signs

Diagnosis

Antiparkinsonian medications – levodopa (dopar, larodopa) with the combination of carbidopa (sinemet)

- Budipine – non-dopaminergic, atiparkinsonian medication (it reduces akinesia, rigidity and tremor)

Anticholinergic therapy – (trihexyphenidyl, cycrimine, procyclidine, biperiden and benztropine mesylate) effective for controlling tremor and rigidity.

Antiviral therapy – amantadine hydrochloride (symmetrel)

- It release dopamine from neuronal sites it has also a low incidence of side effect

Medical management

Dopamine agonist – bromocriptine mesylate (parlodel) and pergolide (permax). Ergot derivatives

- This are dopamine receptor agonist and are useful in postponing the initiation of carbidopa or levodopa therapy.

MAO inhibitors – selegiline (eldepryl)- It inhibits dopamine breakdown and is thought to

slow the progression of the disease.- Selegiline used w/ the combination of dopamine

agonist to delay the use carbidopa or levodopa therapy.

COMT inhibitor (catecol-O-methyltransferase) – comtess and tasmar

- COMT block the enzyme that metabolizes levodopa, amking more levodopa more available for conversion to dopamine in the brain.

Antidepressant – tricyclic antidepressant may be prescribe to alleviate the depression that is so common in parkinson’s disease.

Antihistamine – benadryl, banflex, neo-synephrine have mild central anticholinergic and sedative effects and may reduce tremors.

SURGICAL MANAGEMENTStereotactic procedures – thalamotomy and

pallidotomy are effective in relieving PD symptoms

- pt. with dimentia and atypical parkinson disease are usually not considered for this procedure

- Thalamotomy and pallidotomy is to interrupt the nerve pathways and thereby alleviate tremor or ridigity.

Neural transplantation – surgical implantation of adrenal medulary tissue into the corpus striatum to reestablish normal dopamine release.

Deep brain stimulation – pacemaker like brain implant

- An electrode is placed in the thalamus and connected to a pulse generator implanted in a subcutaneous subclavicular or abdominal pouch. The battery powered pulse generator send high frequency electrical impulses through a wire placed under the skin to a lead anchored to skull

- The electrode blocks nerve pathways in the brain that cause tremors.

THE END