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Understanding the Parkinson's disease


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parkinson's disease pathophysiology, treatment...

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Understanding the Parkinson's disease

  1. 1. Parkinson’s disease by Syed Baseeruddin Alvi (09)
  2. 2. INTRODUCTION • Parkinsonism is a clinical syndrome comprising combinations of motor problems—namely, bradykinesia, resting tremor, rigidity, flexed posture, “freezing,” and loss of postural reflexes. • Studied and discovered by James Parkinson (1817) which he called the shaking palsy and by the Latin term paralysis agitans. • Pathology shows loss of neuromelanin-containing monoamine neurons, particularly dopamine (DA) neurons in the substantia nigra pars compacta.
  3. 3. • Examinations reveals the presence of cytoplasmic eosinophilic inclusions Lewy bodies in monoamine neurons. • The loss of DA content in the nigrostriatal neurons accounts for many of the motor symptoms which is due to neuronal degradation • Six cardinal clinical features of parkinsonism: Tremor at rest Bradykinesia Loss of postural reflexes Rigidity Flexed posture of neck, trunk, and limbs Freezing phenomenon
  4. 4. Concept on pathogenesis of Parkinson’s disease.
  5. 5. The five stages of parkinson’s disease: Stage 1: Unilateral involvement only with minimal or no functional impairment Stage 2: Bilateral or midline involvement, without balance impairment Stage 3: Impairment of righting reflex Stage 4: Fully developed and severely disabling Stage 5: Confinement to bed or wheel chair.
  6. 6. Pathogenesis of PD:
  7. 7. Pathogenesis of PD:
  8. 8. Pathogenesis of PD:
  9. 9. Drugs used in treatment of PD:
  10. 10. Dopamine precursor:  Levodopa (L-DOPA, LARODOPA, L-3,4 dihydroxyphenylalanine), the metabolic precursor of dopamine, is the single most effective agent in the treatment of PD .  It is inert both therapeutic & adverse effects are due to decarboxylation , central and peripheral respectively .  In practice it is always administered in combination with peripherally acting inhibitor of aromatic L-amino acid decarboxylase ( carbidopa , benserazide)
  11. 11. Site of action:
  12. 12. Adverse reactions:  Involuntary muscular twitching of the limbs or facial muscles  muscular spasms most often affecting the tongue, jaw, eyes, and neck  mental changes, such as depression, psychotic episodes, paranoia, and suicidal tendencies.  less serious adverse reactions include anorexia, nausea, vomiting, abdominal pain, dry mouth, difficulty in swallowing, increased hand tremor, headache, and dizziness.
  13. 13. Anticholinergic drugs:  Drugs with anticholinergic activity inhibit acetylcholine (a neurohormone produced in excess in Parkinson’s disease) in the CNS. Drugs with anticholinergic activity are generally less effective than levodopa.
  14. 14. Adverse reactions:  Dry mouth, blurred vision, dizziness, mild nausea, and nervousness.  Other adverse reactions may include skin rash, urticaria urinary retention, tachycardia, muscle weakness, disorientation, and confusion. COMT inhibitors:  These drugs prolong the effect of levodopa by blocking (COMT). When given with levodopa, the COMT inhibitors increase the plasma concentrations and duration of action of levodopa.
  15. 15. Adverse reactions:  Disorientation, confusion, light-headedness, dizziness, dyskinesias, hyperkinesias, nausea, vomiting, hallucinations, and fever  Other adverse reactions are orthostatic hypotension, sleep disorders, excessive dreaming, and muscle cramps Dopamine receptor agonists (non ergot):  It is thought that these drugs act directly on postsynaptic dopamine receptors of nerve cells in the brain, mimicking the effects of dopamine in the brain.
  16. 16. Adverse reactions:  Nausea, dizziness, postural hypotension, hallucinations, somnolence, vomiting, confusion, visual disturbances, abnormal involuntary movements, and headache. Selective MAO-B Inhibitors:  By interfering with one of the enzymes that break down dopamine (monoamine oxidase, or MAO-B), they can enhance and prolong the effect of each dopamine molecule.
  17. 17. Treatment:
  18. 18. Surgical Therapy: