Parkinson s disease

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Parkinson s disease

  1. 1. Parkinson’s Disease
  2. 2. Content  Introduction  Cause and pathogenesis  Case Study: Symptoms Diagnosis Treatment Conclusion
  3. 3. oIntroduction  It is a progressive neurological condition  Results from the degeneration of dopamine- producing neurons in the substantia nigra  Afflicted 25,000 people in Malaysia  Various types of Parkinson’s disease  Risk factors: Middle aged and increased risk with age Hereditary Men (1.5 times more) Environmental exposure to toxins
  4. 4. Symptoms  4 major symptoms: Rigidity – muscles are tensed and contracted Resting tremor – trembling which is most obvious when the patient is at rest or when stressed Bradykinesia – slowness in initiating movement Loss of postural reflexes or instability – poor balance and coordination  Non-motor symptoms Anxiety disorders, depression, sleep disturbances, orthostatic hypotension, olfaction dysfunction, dysphagia, sialorrhoea, dementia, psychosis and visual hallucinations
  5. 5. Diagnosis and Treatment  Diagnosis: Neurological examination Autopsy of brain to find lewy bodies (trademark characteristic) Judgement of physicians  Treatment: Medications Diet Exercise, physical and speech therapy Surgery  Cryothalamotomy  Pallidotomy  Deep brain stimulation
  6. 6. oCauses and Pathogenesis  Degradation of dopaminergic neuron.  Free radicals.  Neurotoxin - MPTP  Genetic factors.
  7. 7. Degradation of Dopaminergic Neuron  Substantia nigra pars compacta.  Death of neuron.  Symptoms of PD don’t appear until 50-80% of the neurons in the pars compacta have died.  Cause of death of neuron is not known.
  8. 8. Free Radicals  Unpaired electrons that can easily react with surrounding molecules and destroy them.  Metabolism of dopamine by MAO produce hydrogen peroxide.  Glutathione normally breaks down the hydrogen peroxide quickly.  Reduced glutathione = loss of protection against free radicals  cell damage
  9. 9. Neurotoxin - MPTP  1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) – neurotoxin.  MPTP crosses the blood-brain barrier and oxidized to 1-methyl-4-phenylpyridinium (MPP+) by monoamine oxidase B (MAO)-B  MPP+ selectively enters dopamine neurons via the dopamine transporter.  MPP+ inhibiting Complex I  leads to cell death via energy deficit.
  10. 10. Genetic Factors • Mutation of SNCA genes in chromosome 4. • 2 types of alterations: • Alanine is replaced with threonine. • Cause alpha-synuclein to misfold. • SNCA genes is inappropriately duplicated or triplicated. • Extra copies of the gene lead to an excess of alpha- synuclein. • Aggregate (Lewy bodies) and attract other protein. • Clog neuron and impair the function of neuron.
  11. 11. oCase Study: • 70 year-old male • Farmer • Referred to a movement disorders outpatient clinic
  12. 12. Symptoms 1. Nondisabling intermittent resting tremor of left hand  Result of pallidal dysfunction  Triggered by specific loss of dopa minergic projections from retrorubral area
  13. 13. 2. Present of myerson  Eyes blinking when tapped on glabella (glabellar reflex)  Involuntary reflex disorder
  14. 14. 3. Mild signs of asymmetrical cogwheel rigidity and bradykinesia (left > right)  Cause to muscular aches and sensation of fatigue  Face become masklike, opened mouth, drooling and reduced blinking  Underscaling of movement commands in internally generated movements  Reflect the role of the basal ganglia in selecting and reinforce appropriate patterns of cortical activity during movement preparation and performance
  15. 15. 4. Normal gait and balance and postural reflexes  Under activity in the left cerebellar hemisphere with contrast of over activity in vermis  Associated with loss of lateral gravity shift in parkinsonian gait  Loss of postural reflexes  No tendency of falling forward  No difficulty of walking, turning and stopping
  16. 16. Diagnostic Test  No specific test.  Usually based on present of symptoms.  Referral time should not be more than 6 weeks and not exceed two weeks in severe case.  No specific lab test used for diagnosis.  Follow – up= every 6 to 12 months.
  17. 17.  Suggested method include: Neurologic examination Oculomotor examination Electroencephalograms (EEG) Single photon emission computed tomography (SPECT)
  18. 18.  Neurological examination Patient’s medical and family history Observe sign and symptoms present. Suggested symptoms include:  Bradikinesia  Tremor  Hypokinesia  Rigidity Patient had normal cognition and myerson sign is present. Intermittent mild tremor was observed as well as cogwheel rigidity and bradykinesia.
  19. 19.  Oculomotor examination To check abnormalities of eye movement, generation, and control. Normal in patient.  Single photon emission computed tomography (SPECT) Show dramatic (50%) loss of striatal uptake in patient compared to normal individual. Electroencephalograms Record patient’s brain electrical activity.
  20. 20. Single photon emission computed tomography (SPECT)
  21. 21. Treatment According to the case study the patient was on initiation of treatment:In early-stage disease, the pharmacological options for the treatment of PD are multiple.  Levodopa:  is a medicine that the brain converts to dopamine. is a medicine used to control symptoms of Parkinson's disease and used at all stages of the disease. Levodopa does not slow the disease process, but it improves muscle movement and delays severe disability. long-term levodopa therapy within 5 to 10 years can cause complication to occur such as Dyskinesia.
  22. 22.  Dopamine agonist: Example of drugs:pramipexole,ropinirole directly stimulate the receptors in nerves in the brain that normally would be stimulated by dopamine. used in the early stages of Parkinson’s disease to reduce symptoms. effective in people who have been newly diagnosed with the disease (especially those younger than 60). Not effective as levodopa in reducing symptom but can prevent long term effect caused by levodopa.
  23. 23.  Monoamine oxidase type B inhibitor MAO-B is an enzyme in our brain that naturally breaks down several chemicals in our brain including dopamine. Prevent the breakdown dopamine. they prevent the removal of dopamine between nerve endings and enhance release of dopamine from nerve cells. Example of drug: Rasagiline and selegiline. used in the early stages, to treat very mild symptoms (such as resting tremor) and delay the need for levodopa. rasagiline or selegiline may be added to levodopa treatment to reduce motor fluctuations , increase the time of effect of the levodopa.
  24. 24.  Amantadine  treat people who are in the early stages of Parkinson's disease.  It is best used in people who have mild to moderate symptoms. cause greater amounts of dopamine to be released in the brain. can be used with levodopa in the later stages of Parkinson's disease to reduce dyskinesias.
  25. 25.  Anticholinergic Example of drugs: benztropine,biperiden Anticholinergic medicines decrease levels of acetylcholine to achieve a closer balance with dopamine levels. In order to reduce the symptom.
  26. 26. Treatment In Malaysia Decision pathway for the initiation of medication
  27. 27.  Levodopa ( L-Dopa) the most effective antiparkinsonian medication. “start low, go slow” approach, L-dopa can be started at a dose of 50 mg daily (e.g., ¼ tablet of Madopar® 200/50 mg) increasing every 3-7 days by 50 mg to an initial maintenance dose of 50-100 mg 3x daily.  Selegiline ( Jumex and Selegos) usual dose is 10 mg in the morning. has a mild antiparkinsonian effect.
  28. 28.  Dopamine agonist Next most potent class of drug after L-dopa. Dopamine agonist Usual Starting Dose Maximum recommende d Dose Piribedil (Trivastal Retard *) 25-50mg 300mg/d Ropinirole immidiate release ( Requip *) 0.25mg 24mg/d Ropinirole Prolong Release (Requip PD*) 2mg 24mg/d
  29. 29.  Anticholinergic agents  These include trihexyphenidyl or benzhexol (Apo- Trihex® and Benzhexol®)(1 or 2 mg 2-3x daily) and orphenadrine (Norflex®) (50 mg 2-3x daily).  Non-Pharmocologic Management physiotherapy: stretching and strengthening exercises and balance training. occupational therapy: lifestyle adaptations and assessment of safety in the home environment. speech therapy: rehabilitation techniques to strengthen speech for improved communication. Dietitian: advice from them.
  30. 30. Conclusion  Patient has idiopathic Parkinson’s disease  There is no cure but therapies are available  Treatments aim to: Prevent clinical progression Improvement of parkinsonism Delay of motor complications  Complications: choking, falls and side effects of drugs  Prognosis: normal life expectancy for treated patients
  31. 31. Reference Anonymous. (2012). Tremor Fact Sheet. [Online]. Available from: http://www.ninds.nih.gov/disorders/tremor/detail_tremor.htm.Nati onal, Institute of Neurological Disorders and Stroke. Accessed on 2nd March 2013 Dr Ananya Mandal, MD. (2013). Parkinson's Disease Pathophysiology. [Online]. Available from: http://www.news- medical.net/health/Parkinsons-Disease-Pathophysiology.aspx. [Accessed on 1st March 2013]. Dr. Ananya Mandal. (2013). Parkinson’s disease Prognosis. [Online]. Available from: http://www.news- medical.net/health/Parkinsons-Disease-Prognosis.aspx. [Accessed on 2nd March 2013]. Malaysian Parkinson’s Disease Association. (2012). Association wants Disability Rights for Parkinson’s Patients. [Online]. Available from: http://mpda.org.my/article.php?type=news&9ja847hd0a1=144. [Accessed on 2nd March 2013].
  32. 32. Mayo Clinic. Parkinson’s Disease: Risk Factors. [Online]. Available from: http://www.mayoclinic.com/health/parkinsons- disease/DS00295/DSECTION=risk-factors. [Accessed on 1st March 2013]. Parkinson’s Disease Society. The professional’s guide to Parkinson’s Disease. [Online]. Available from: http://www.parkinsons.org.uk/pdf/B126_Professionalsguide.pdf. [Accessed on 1st March 2013]. Parkinson’s UK. Types of Parkinson’s and parkinsonism. Online]. Available from: http://www.parkinsons.org.uk/about_parkinsons/what_is_parkins ons/types_of_parkinsons.aspx. [Accessed on 2nd March 2013]. Public Health and Genetics Information Series. Parkinson’s disease. [Online]. Available from: http://www.hgen.pitt.edu/counseling/public_health/parkinsons.pdf . [Accessed on 1st March 2013]. Robert A Hauser, MD. (2013). Parkinson Disease . [Online]. Available from : http://emedicine.medscape.com/article/1831191- overview#aw2aab6b2b1aa.[Accessed 1st March 2013].
  33. 33. Takashi Hanakawa. (1999). Mechanisms underlying gait disturbance in Parkinson's disease. [Online]. Available from : http://brain.oxfordjournals.org/content/122/7/1271.full. [Accessed on 2nd March 2013] Ted K Koutouzis, MD. (2005). Parkinson's Disease. [OnlineAvailable from : http://www.emedicinehealth.com/parkinson_disease/article _em.htm. [Accessed 1st March 2013]. University of Maryland Medical Centre. Diagnosing Parkinson’s Disease. [Online]. Available from: http://www.umm.edu/parkinsons/diagnosis.htm. [Accessed on 1st March 2013]. Wooten. G.F., Currie. L.J., Bovbjerg. V.E., Lee.J.K. and Patrie. J. (2013). Are men at greater risk for Parkinson’s disease than women? J Neurol Neurosurg Psychiatry. 75:637-639.

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