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Parkinson’s disease Dr. Osman Sadig Bukhari
<ul><li>Parkinson’s disease is an idiopathic </li></ul><ul><li>progressive degenerative disease of the </li></ul><ul><li>d...
<ul><li>Prevalence </li></ul><ul><li>- world wide </li></ul><ul><li>- 1: 1000 general population increasing sharply </li><...
<ul><li>Pathology </li></ul><ul><li>- progressive degeneration with eosinophilic </li></ul><ul><li>inclusion bodies ( Lewy...
<ul><li>Clinical features </li></ul><ul><li>- Symptoms develop over moths & several years </li></ul><ul><li>1-Pill rolling...
<ul><li>4- Stooping posture, festinant & shuffling </li></ul><ul><li>gait wz reduced limb swinging </li></ul><ul><li>Propu...
 
<ul><li>10- Power remains normal, reflexes may </li></ul><ul><li>be increased, planters remain flexor </li></ul><ul><li>an...
<ul><li>Diagnosis </li></ul><ul><li>- characteristic clinical picture </li></ul><ul><li>- careful history & examination to...
<ul><li>6- Progressive supranuclear palsy </li></ul><ul><li>7- Multiple system atrophies: </li></ul><ul><li>- Olivo – pont...
<ul><li>Management of Parkinson’s disease </li></ul><ul><li>A- identify 2ry causes of parkinsonism & TR </li></ul><ul><li>...
<ul><li>1- Dopaminergic drugs act through </li></ul><ul><li>- replacement of neuronal dopamine e.g </li></ul><ul><li>L dop...
<ul><li>** drug induced parkinsonism is best treated  by  anti muscarinic drugs & not by L dopa since </li></ul><ul><li>ne...
<ul><li>therapeutic doses to avoid large doses of L dopa </li></ul><ul><li>e.g Sinemet ( cabidopa + L dopa 1 : 10) : </li>...
<ul><li>2-  Amantadine </li></ul><ul><li>- anti viral </li></ul><ul><li>- less effective than L dopa but may  </li></ul><u...
<ul><li>3-  Bromocriptine </li></ul><ul><li>- dopamine receptor agonist </li></ul><ul><li>- ½ life 5hrs, therefore smoothe...
<ul><li>4-  Selegline </li></ul><ul><li>- selective B MAO-I </li></ul><ul><li>- It delays break down of dopamine & prolong...
<ul><li>5-  Entacapone </li></ul><ul><li>- COMT inhibitor </li></ul><ul><li>- Used to reduce end- of- dose fluctuation </l...
<ul><li>- trihexyphenidyl (benzhexol 2mg), benz atropin </li></ul><ul><li>orphenadrine.   </li></ul>
<ul><li>3-  General management of parkinsonism </li></ul><ul><li>- Positive attitude by encouraging physical </li></ul><ul...
<ul><li>- long term therapy is associated with:  </li></ul><ul><li>1- end- of- dose fluctuation= swings  from early mornin...
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Parkinson’S Disease

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Transcript of "Parkinson’S Disease"

  1. 1. Parkinson’s disease Dr. Osman Sadig Bukhari
  2. 2. <ul><li>Parkinson’s disease is an idiopathic </li></ul><ul><li>progressive degenerative disease of the </li></ul><ul><li>dopaminergic neurones in za substantia </li></ul><ul><li>nigra resulting in: </li></ul><ul><li>1- Bradykinesia or akinesia </li></ul><ul><li>2- Resting tremors </li></ul><ul><li>3- Muscle rigidity causing restricted </li></ul><ul><li>mobility </li></ul>
  3. 3. <ul><li>Prevalence </li></ul><ul><li>- world wide </li></ul><ul><li>- 1: 1000 general population increasing sharply </li></ul><ul><li>over the age of 60. </li></ul><ul><li>- M> F </li></ul><ul><li>Aetiology </li></ul><ul><li>- unknown </li></ul><ul><li>- no infective agent </li></ul><ul><li>- no enviromental factor ( dis world wide) </li></ul><ul><li>- ? Less in tobacco smokers (nicotine) </li></ul><ul><li>- ? MPTP, a pyridine cpd cause similar syndrome </li></ul><ul><li>( enviromental MPTP like herbicide?) - ? Genetic factors, clusters of early onset Parkinson’s </li></ul><ul><li>in some families ? Mutation in parkin gene on </li></ul><ul><li>chromosome 6 </li></ul>
  4. 4. <ul><li>Pathology </li></ul><ul><li>- progressive degeneration with eosinophilic </li></ul><ul><li>inclusion bodies ( Lewy bodies) in za neurones </li></ul><ul><li>of substantia nigra & other basal ganglia nuclei </li></ul><ul><li>- loss of melanin & dopamine that correlate with the degree of akinesia </li></ul><ul><li>- imbalance between dopaminergic & cholinergic </li></ul><ul><li>neurotransmitters. </li></ul>
  5. 5. <ul><li>Clinical features </li></ul><ul><li>- Symptoms develop over moths & several years </li></ul><ul><li>1-Pill rolling tremors of za hands, often unilateral, is the most common initial feature. It is eventually becomes bilateral involving the UL, LL & jaw. It diminishes on voluntary movement an increases by emotion. </li></ul><ul><li>2- Slowness of movement or bradykinesia is </li></ul><ul><li>usually by za family. There is difficulty in </li></ul><ul><li>initiating movements including fine finger move </li></ul><ul><li>3- Rigidity causes stiffness . It is lead pipe and </li></ul><ul><li>cogwheel rigidity. </li></ul>
  6. 6. <ul><li>4- Stooping posture, festinant & shuffling </li></ul><ul><li>gait wz reduced limb swinging </li></ul><ul><li>Propulsion & retropulsion are characteri </li></ul><ul><li>There is postural instability & falls. </li></ul><ul><li>5- Masked expressionless face wz reduced </li></ul><ul><li>blinking. </li></ul><ul><li>6- Monotonous speech progressing to </li></ul><ul><li>slurring & eventually lost. </li></ul><ul><li>7- Micrographia </li></ul><ul><li>8- Drooling of saliva, dysphagia, constipati </li></ul><ul><li>urinary troubles </li></ul><ul><li>9- Excessive sweating & greasy skin. </li></ul>
  7. 8. <ul><li>10- Power remains normal, reflexes may </li></ul><ul><li>be increased, planters remain flexor </li></ul><ul><li>and sensations are normal. </li></ul><ul><li>11- Cognitive fns preserved at least early, </li></ul><ul><li>dementia develops in late stages, </li></ul><ul><li>anxiety & depression are common </li></ul><ul><li>12- No remission & za rate of progression </li></ul><ul><li>is variable wz death resulting from </li></ul><ul><li>chest infection, UTI & bed sores </li></ul>
  8. 9. <ul><li>Diagnosis </li></ul><ul><li>- characteristic clinical picture </li></ul><ul><li>- careful history & examination to exclude other </li></ul><ul><li>causes of Akinetic – rigid syndromes i.e. </li></ul><ul><li>secondary causes of parkinsonism </li></ul><ul><li>1- Drug induced parkinsonism e.g neuroleptics, </li></ul><ul><li>reserpine, methyldopa, tricyclic antidepressants </li></ul><ul><li>mainly cause slowness & rigidity wz little tremor </li></ul><ul><li>2- Post encephalitis lethargica </li></ul><ul><li>3- Toxins e.g MPTP, CO, Mn </li></ul><ul><li>4- CVAs, hypoparathyroidism, trauma & SOL </li></ul><ul><li>5- Wilson’s disease & athetoid C. palsy in childr </li></ul>
  9. 10. <ul><li>6- Progressive supranuclear palsy </li></ul><ul><li>7- Multiple system atrophies: </li></ul><ul><li>- Olivo – ponto – cerebellar degeneration </li></ul><ul><li>- Pry autonomic failure ( Shy Drager syndr) </li></ul><ul><li>8- Alzeheimer disease </li></ul><ul><li>9- Huntington's chorea </li></ul>
  10. 11. <ul><li>Management of Parkinson’s disease </li></ul><ul><li>A- identify 2ry causes of parkinsonism & TR </li></ul><ul><li>e.g withdrawal of neuroleptics, penicillamine </li></ul><ul><li>for Wilson’s. </li></ul><ul><li>B- Drug therapy to restore dopaminergic/ </li></ul><ul><li>cholinergic balance, but </li></ul><ul><li>- not curative </li></ul><ul><li>- greatly improve za quality of life </li></ul><ul><li>- should only be started when za functional </li></ul><ul><li>disability interferes wz life. </li></ul>
  11. 12. <ul><li>1- Dopaminergic drugs act through </li></ul><ul><li>- replacement of neuronal dopamine e.g </li></ul><ul><li>L dopa which is za natural precursor of </li></ul><ul><li>dopamine & crosses BBB ( dopamine not) </li></ul><ul><li>- releasing dopamine from its stores and </li></ul><ul><li>inhibiting its re uptake e.g amantadine </li></ul><ul><li>- prolonging za action of dopamine by selectiv </li></ul><ul><li>inhibition of its metabolism e.g selegline </li></ul><ul><li>- dopamine receptor agonists e.g bromocriptine </li></ul><ul><li>2- Anti muscarinic anti cholinergics reduce </li></ul><ul><li>cholinergic activity by inhibiting acetyl choline </li></ul><ul><li>esterase e.g benzhexol. </li></ul>
  12. 13. <ul><li>** drug induced parkinsonism is best treated by anti muscarinic drugs & not by L dopa since </li></ul><ul><li>neuroleptic drugs block dopamine receptors. </li></ul><ul><li>Individual drugs </li></ul><ul><li>1- Levodopa (L dopa ) </li></ul><ul><li>- a a precursor of dopamine wz short ½ life 1,5h </li></ul><ul><li>- dopamine can not be used as it is rapidly </li></ul><ul><li>destroyed peripherally (gut, liver & blood) by </li></ul><ul><li>MAO inhibitor & catechol O –methyl transferase </li></ul><ul><li>and does not cross BBB. </li></ul><ul><li>- peripheral dopa decarboxylase inhibitors which </li></ul><ul><li>do not cross BBB are combined with L dopa in </li></ul>
  13. 14. <ul><li>therapeutic doses to avoid large doses of L dopa </li></ul><ul><li>e.g Sinemet ( cabidopa + L dopa 1 : 10) : </li></ul><ul><li>110, 250mg. OR Madopar ( benserazide + L dop </li></ul><ul><li>1:4: 65.5, 125, 250mg. </li></ul><ul><li>- With combination low doses of L dopa are used </li></ul><ul><li>and side effects are reduced: </li></ul><ul><li>(N, V, post hypotension, arrhythmias, dyskin </li></ul><ul><li>confusion, agitation, hallucination, depressio </li></ul><ul><li>long term problems of end of dose deterior </li></ul><ul><li>and on off swings) </li></ul><ul><li>- L dopa interaction wz non selective MAO-I </li></ul><ul><li>causes hypertensive crisis. In this situation L dopa dopamine Noradrenaline HT. </li></ul>
  14. 15. <ul><li>2- Amantadine </li></ul><ul><li>- anti viral </li></ul><ul><li>- less effective than L dopa but may </li></ul><ul><li>enhance its effect </li></ul><ul><li>- mainly used in early mild cases </li></ul><ul><li>- dose: 100-300mg/d </li></ul><ul><li>- SE= post hypot, ankle edema & livedo </li></ul><ul><li>reticularis. </li></ul>
  15. 16. <ul><li>3- Bromocriptine </li></ul><ul><li>- dopamine receptor agonist </li></ul><ul><li>- ½ life 5hrs, therefore smoother action than </li></ul><ul><li>L dopa & no fluctuation in action </li></ul><ul><li>- dose: 10-80mg starting wz 1.25mg e.g </li></ul><ul><li>Parlodel (2.5 &10mg) </li></ul><ul><li>- used in long term L dopa problems </li></ul><ul><li>- SE= similar to L dopa. </li></ul>
  16. 17. <ul><li>4- Selegline </li></ul><ul><li>- selective B MAO-I </li></ul><ul><li>- It delays break down of dopamine & prolongs </li></ul><ul><li>its action </li></ul><ul><li>- main use in those wz long term L dopa </li></ul><ul><li>problems e.g end of dose deterioration </li></ul><ul><li>- anti depressant also </li></ul><ul><li>- e.g eldepryl 5mg X2. SE= similar to L dopa. </li></ul><ul><li>- no hypertensive cheese reaction (tyramine) </li></ul><ul><li>which occur wz non selective MAO-I which </li></ul><ul><li>prevent degradation of dietary amines by </li></ul><ul><li>MAO-I. Tyramine is degraded by type A MAO-I </li></ul>
  17. 18. <ul><li>5- Entacapone </li></ul><ul><li>- COMT inhibitor </li></ul><ul><li>- Used to reduce end- of- dose fluctuation </li></ul><ul><li>in response to L dopa. </li></ul><ul><li>6- Anti muscarinic anti cholinergics </li></ul><ul><li>- Act by blocking Ach in za CNS restoring the </li></ul><ul><li>imbalance created by decreased dopaminergi </li></ul><ul><li>activity. </li></ul><ul><li>- most effective in drug induced parkinsonism and in mild cases sp. tremor, rigidity and sialorrhMoea. Not used I n > 65, glucoma & BPH. SE= those of anti cholinergics. </li></ul>
  18. 19. <ul><li>- trihexyphenidyl (benzhexol 2mg), benz atropin </li></ul><ul><li>orphenadrine. </li></ul>
  19. 20. <ul><li>3- General management of parkinsonism </li></ul><ul><li>- Positive attitude by encouraging physical </li></ul><ul><li>activity, physiotherapy & speech therapy </li></ul><ul><li>- Early mild cases: anti muscarinic & amantadine </li></ul><ul><li>-With progression of za disease dose of L dopa </li></ul><ul><li>needs to be increased wz more SEs which may </li></ul><ul><li>be overcome by reducing individual doses </li></ul><ul><li>and increasing za frequency of administration or </li></ul><ul><li>by using bromocriptine & selegline </li></ul><ul><li>- L dopa + carbidopa restore near normal </li></ul><ul><li>physical activity in 75%. Ultimately higher doses are required. </li></ul>
  20. 21. <ul><li>- long term therapy is associated with: </li></ul><ul><li>1- end- of- dose fluctuation= swings from early morning akinesia to peak </li></ul><ul><li>dose dyskinesia. </li></ul><ul><li>2- on- off swings= random fluctuation </li></ul><ul><li>from mobility to dyskinesia wz peak </li></ul><ul><li>plasma conc. </li></ul><ul><li>- Long term problems wz L dopa is treated </li></ul><ul><li>by: - gradual & partial substitution of </li></ul><ul><li>L dopa wz bromocriptine & selegline </li></ul><ul><li>effective in end- of- dose deterioration </li></ul><ul><li>- decreasing dose of L dopa & shortening za interval between doses. </li></ul>
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