Parkinson diseases

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Parkinson diseases

  1. 1. PRESENTED BY- NAVEEN KADIAN DEPARTMENT OF PHARMACEUTICAL CHEMISTRY K.L.E’S COLLEGE OF PHARMACY BELGAUM-10
  2. 2. CONTENTS • Introduction • Epidemiology of PD • Causes of Parkinsonism • Risk factors of PD • Clinical features of PD • Treatment • Reference
  3. 3. Definition • Neurodegenerative disease is a condition which affects brain function. Neurodegenerative diseases result from deterioration of neurons. • They are divided into two groups: – conditions causing problems with movements – conditions affecting memory and conditions related to dementia. – Examples: • Alzheimer’s • Parkinson’s • Huntington’s • Creutzfeldt-Jakob disease • Multiple Sclerosis • Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease)
  4. 4. Risk Factors • Known – Certain genetic polymorphisms – Increasing age Possible Gender Poor education Endocrine conditions Oxidative stress Inflammation Stroke Hypertension Diabetes Head trauma Depression Infection Tumors Vitamin deficiencies Immune and metabolic conditions Chemical exposure Smoking??
  5. 5. PARKINSON`S DISEASE is movement disorder of unknown etiology due to degeneration of neurons in the nigrostrial dopamine system. History: First described in 1817 by an English physician, James Parkinson, in “An Essay on the Shaking Palsy.” The famous French neurologist, Charcot, further described the syndrome in the late 1800s.
  6. 6. Epidemiology of PD The most common movement disorder affecting 1-2 % of the general population over the age of 65 years. The second most common neurodegenerative disorder after Alzheimer s disease (AD).
  7. 7. Causes of Parkinsonism • Impaired release of dopamine- Idiopathic parkinsonism. • Drug depleting dopamine store-reserpine, tetrabenzine. • Toxin damaging dopaminergic neuron. • Viral infection- Encephalitis ,Japanese encephalitis • Trauma-repeated head injury[punch drunk syndrome] • Miscellaneus-wilson disease,huntingtion,s disease
  8. 8. Dopamine pathways in human brain
  9. 9. Dopamine synthesis
  10. 10. Risk factors of PD  Age - the most important risk factor  Positive family history  Male gender  Environmental exposure: Herbicide and pesticide exposure, metals (manganese, iron), well water, farming, rural residence, wood pulp mills; and steel alloy industries  Race  Life experiences (trauma, emotional stress, personality traits such as shyness and depressiveness)?  An inverse correlation between cigarette smoking and caffeine intake in case-control studies.
  11. 11. Clinical features of PD • Three cardinal symptoms:  resting tremor  bradykinesia (generalized slowness of movements)  muscle rigidity
  12. 12. CLINICAL FEATURE • TREMORS(4-6hz): • tremors[pill rolling] at rest, decreases on action. Usually first in finger/thumb. • Coarse flexion/extension of finger[pill rolling & drum beating] • RIGIDITY- • Cog wheel type especially in upper limb {stiffness in all direction of movement}. • Plastic type {lead type} mostly appreciated in legs. In trunk rigidity manifest by flexed& stooped posture
  13. 13. Hypokinesis • Charactrized by poverty & slowness of movement. Slowness in initiating movement. Handwriting micrographia. • GAIT-patient walk with short step , with a tendency to run{as they are catching their own centre of gravity}-festinating gait • General-expressionless face with staring look with infrequent blinking. Monotonus speech. Dementia & Depression in advance stage
  14. 14. Drugs used to treat Parkinson’s Disease
  15. 15. TREATMENT • Anticholinergic drug- to relieve tremors. • Dopamine agonist- bromocriptine& pergolide. • Amantadine-potentiate release of dopamine. • Selegeline : early stage, neuroprotective, delay neuronal degeneration. • Levodopa & carbidopa
  16. 16. Therapy of PD: levodopa  Late 1950s: L-dihydroxyphenylalanine (L-DOPA; levodopa), a precursor of DA that crosses the blood-brain barrier, could restore brain DA levels and motor functions in animals treated with catecholamine depleting drug (reserpine).  First treatment attempts in PD patients with levodopa resulted in dramatic but short-term improvements; took years before it become an established and succesfull treatment.  Still today, levodopa cornerstone of PD treatment; virtually all the patients benefit.
  17. 17. Therapy of PD: limitations of levodopa  Efficacy tends to decrease as the disease progresses.  Chronic treatment associated with adverse events (motor fluctuations, dyskinesias and neuropsychiatric problems).
  18. 18. Inhibition of peripheral COMT by entacapone increases the amount of L-DOPA and dopamine in the brain and improves the alleviation of PD symptoms.
  19. 19. Therapy of PD: limitations of levodopa  Does not prevent the continuous degeneration of nerve cells in the subtantia nigra, the treatment being therefore symptomatic.
  20. 20. Therapy of PD: Other treatments DA receptor agonists: Bromocriptine Pergolide
  21. 21. ropinirole cabergoline
  22. 22. Anticholinergics: Amantadine AntiHistamines: Diphenhydramine Orphenadrine Selegiline
  23. 23. Antidepressant Miscellanous: imipramine nortriptyline Benzotropine procyclidine
  24. 24. References  BURGER’S Medicinal Chemistry & Drug discovery,6th Edn,vol-1, Wiley-interscience publication  CORWIN HANSCH, Comprehensive Medicinal Chemistry,vol –IV 2008,Pregamon press  Principles of Medicinal Chemistry by William O.Foye  Medicinal Pharmacology by K.D Triphati.  http:// www.cpharm.ucsf.edu/ kuntz/doct.html  http:// www.bmm.icnet.uk/ ftdock/ftdoc.html  www. Wikepedia.com  www. Google.com  www. Ipasp . com

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