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Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
Parkinson s disease
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Parkinson s disease

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  • 1. Parkinson’s Disease
  • 2. Content  Introduction  Cause and pathogenesis  Case Study: Symptoms Diagnosis Treatment Conclusion
  • 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. 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. 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. oCauses and Pathogenesis  Degradation of dopaminergic neuron.  Free radicals.  Neurotoxin - MPTP  Genetic factors.
  • 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. 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. 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. 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. oCase Study: • 70 year-old male • Farmer • Referred to a movement disorders outpatient clinic
  • 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. 2. Present of myerson  Eyes blinking when tapped on glabella (glabellar reflex)  Involuntary reflex disorder
  • 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. 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. 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.  Suggested method include: Neurologic examination Oculomotor examination Electroencephalograms (EEG) Single photon emission computed tomography (SPECT)
  • 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.  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. Single photon emission computed tomography (SPECT)
  • 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.  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.  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.  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.  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. Treatment In Malaysia Decision pathway for the initiation of medication
  • 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.  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.  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. 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. 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. 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. 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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