Parkinson diseases

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  • 2. CONTENTS • Introduction • Epidemiology of PD • Causes of Parkinsonism • Risk factors of PD • Clinical features of PD • Treatment • Reference
  • 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. 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. 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. 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. 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. Dopamine pathways in human brain
  • 9. Dopamine synthesis
  • 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. Clinical features of PD • Three cardinal symptoms:  resting tremor  bradykinesia (generalized slowness of movements)  muscle rigidity
  • 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. 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. Drugs used to treat Parkinson’s Disease
  • 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. 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. 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. 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. 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. Therapy of PD: Other treatments DA receptor agonists: Bromocriptine Pergolide
  • 21. ropinirole cabergoline
  • 22. Anticholinergics: Amantadine AntiHistamines: Diphenhydramine Orphenadrine Selegiline
  • 23. Antidepressant Miscellanous: imipramine nortriptyline Benzotropine procyclidine
  • 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:// kuntz/doct.html  http:// ftdock/ftdoc.html  www.  www.  www. Ipasp . com