Prakash park


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parkinson's disease by me ..........prakash mahala p.g. medical surgical nursing at himalayan college of nursing

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Prakash park

  1. 1. Parkinson’s Disease BY:- PRAKASH MAHALA M.SC.NURSING 1STYEAR
  2. 2. Introduction:- Dr. James Parkinson (1755-1828)  “involuntary tremulous motion”  “shaking palsy”  London home
  3. 3. The disease was firstdescribed in 1817 by a Britishphysiciannamed James ParkinsonHe wrote "An Essay onShaking Palsy"
  4. 4.  Progressive loss of substantia nigra dopaminergic neurons; loss of 70% before one is symptomatic, >90% loss at death  Disorder that affects the central nervous system:  Progressively  Debilitating  Degeneratively  Easily characterized by decreased movement, muscular rigidity, resting tremors, and postural instability
  5. 5.  Progressive neurodegenerative disorder that causes motor and nonmotor dysfunction – Characterized by loss of dopaminergic neurons in substantia nigra . – Can affect other areas of the nervous system including the autonomic and enteric nervous systems. Second most common neurodegenerative disorder after Alzheimer’s disease
  6. 6. Definition :- Parkinsons disease is a progressive, neurodegenerative disorder that affects movement, muscle control, and balance as well as numerous other functions. It is part of a group of conditions known as motor systems disorders. it is always chronic and progressive, meaning that the symptoms always exist and always worsen over time.
  7. 7. Incidence :- Prevalence Rate : 200 per 100,000 Rare for individuals < 40 years of age 1% for individuals > 60 years of age 2% for individuals > 85 years of age Men > Women Incidence rate : 20 per 100,000 (annually)The National Parkinson’s Foundation estimates that up to 1.5 million Americans have the diseaseApproximately 50,000 new cases are diagnosed each year
  8. 8. Type :- There are three types of Parkinsons disease and they are grouped by age of onset: Adult-Onset Parkinsons Disease - This is the most common type of Parkinsons disease. The average age of onset is approximately 60 years old. The incidence of adult onset PD rises noticeably as people advance in age into their 70s and 80s.
  9. 9.  Young-Onset Parkinsons Disease - The age of onset is between 21-40 years old. Though the incidence of Young-Onset Parkinsons Disease is very high in Japan (approximately 40% of cases diagnosed with Parkinsons disease). Juvenile Parkinsons Disease - The age of onset is before the age of 21. The incidence of Juvenile Parkinsons Disease is very rare.
  10. 10. STAGES OFPARKINSON’S DISEASE EARLY - no functional impairment MILD - honeymoon period MODERATE - multiple drugs, occupational and social activities affected SEVERE - side effects from drugs, resistant to therapy, reduced quality of life LATE - wheelchair or bed bound
  11. 11. Etiology:- Increasing age (rare in those < 50; early or young onset) 2 times more common in men than women may be more common in whites 1.4 to 3.5 more often to occur in families with relatives with PD Environmental factors (pesticides, rural residence)
  12. 12.  Head trauma Encephalitis has been clearly associated with parkinsonism.
  13. 13. Pathophysiology:- The basal ganglia is an important part of the motor system. It is made up of the caudate nucleus, the putamen, and the globus pallidus. The caudate nucleus and the putamen connect with the globus pallidus which connects with the motor cortex through the ventral anterior and ventrolateral nuclei of the thalamus.
  14. 14. The basal ganglia receives its most important input from the substantia nigra.The substantia nigra has dopaminergic neurons that release dopamine to the caudate and the putamen.In normal movement, the substantia nigra releases dopamine to the caudate and putamen which then produce a balance between excitatory and inhibitory effects to the globus pallidus internal and glosbus pallidus external, respectively.
  15. 15. Overall, for both pathways there is an excitatory effect, so the input of dopamine from the substantia nigra is very important for facilitating movement.When there is damage to the dopaminergic neurons of the substantia nigra the above pathways are disrupted and the symptoms of Parkinson’s comes up.
  16. 16. Symptoms:- Due to the lack of dopamine (neurotransmitters) brain signals to the body are hindered. Therefore symptoms may include:  Tremores occurring in the limbs, jaws and face  Bradykinesia (slow movement)  Impaired balance and coordination  Stiffness of the limbs and trunk
  17. 17.  Secondary Symptoms: Varies for different persons caused by eventual loss of both voluntary and involuntary controls of the nervous system.  Small, cramped penmanship (micrographia)  Scaling of the skin (seborrhea)  Loss of bodily waste management (incontinence)  Dementia
  18. 18.  Feelings of anxiety, depression and loneliness. Excessive salivation (hypersalivation) and excessive sweating Constipation Soft, whispery voice (hypophonia) Slow response to questions (bradyphrenia)
  19. 19. Common Treatments:Medication:- Levodopa and Carbidopa  this substance is converted into dopamine by an enzyme dopa decarboxylase (DDC) that exists in the nervous system. Unfortunately, most of the levodopa is metabolized before reaching the brain1.  Actual dopamine can’t be used because it is unable to cross the cell walls into the brain.  Carbidopa is used in conjuction with Levodopa to increase the amount of Levodopa to enter the brain.  Most effective against bradykinesia and rigidity  Ineffective against balance problems
  20. 20. COMT = catechol-O-methyltransferase; MAO-B = monoamine oxidase B
  21. 21.  Amantadine  An antiviral drug with dopamine agonist properties  Increases the release of dopamine  Used for early treatment  loses effectiveness in 3-4 months Selegiline  Prevents the breakdown of natural and levodopa dopamine by inhibiting the enzyme monoamine oxidase B (MAO-B, metabolizes dopamine in the brain)  Delay the need for levodopa and carbidopa treatment for a year
  22. 22.  Anticholinergics  Main treatment for tremors before levodopa but the side effects overwhelmed the benefits  Side effects include dry mouth, urine retension, nausea, and mental problems.
  23. 23. Common Treatments: Surgery Thalamotomy  Destruction of small amounts of thalamus tissue  Done on one half of the brain because it usually cause slurred speech and lack of coordination  Controls tremors Pallidotomy  Electric current is used to destroy a little bit of tissue in the globus pallidus  May improve tremor, rigidity and slowed movement by interrupting the neural pathway between the globus pallidus and the thalamus  Counter involuntary movements caused by drug treatments  Not a cure, benefits may not last  The surgery carries a number of risks like slurred speech, disabling weakness and vision problems2
  24. 24.  Deep Brain Stimulation  There is an extravagant amount of PD research going on. Alot of it centers around Deep Brain Stimulation.  A brain implant device that is now widely used to help control many of the symptoms of Parkinsons disease  This procedure rarely causes brain hemorrhage and stroke-like problems  Infection is a risk and may require parts of the device to be replaced. For example, the batteries requires replacement every few years.  Deep brain stimulation isnt beneficial for people who dont respond to carbidopa-levodopa. And the device isnt for people who already have serious difficulty with thinking and memory because it may make those symptoms worse.
  25. 25.  Picture of electrode in sub-thalemic nucleus
  26. 26. Sources
  27. 27. Nursing management :- Nursing interventions for each of the symptoms of Parkinsons disease, muscle rigidity, bradykinesia, tremors at rest and postural reflex abnormalities, are designed to increase the patients quality of life by minimizing symptoms. Nurses are responsible for planning patient medication schedules to maximize drug effectiveness.
  28. 28.  Constipation is addressed by increasing the patients fibre and fluid intake and by increasing the patients mobility. Patient mobility is increased when the patient is taught purposeful activities and to concentrate on the way he walks. Communication is facilitated if the patient takes deep breaths before speaking and uses diaphragmatic speech.
  29. 29.  Dietary implications include a low-proteinregimen for the patient during the day, eliminatingfoods high in Vitamin B6, high caloric foods, andsoft-solid foods offered at frequent feedings.
  30. 30. COMPLICATIONS:- Motor fluctuations Dyskinesis Posture, gait, falling Neuropsychiatric problems Sleep disorders Sensory phenomena Dysautonomias Speech disturbances
  31. 31. Summary:- Because PD is a progressive disorder, early diagnosis and treatment intervention with neuroprotective therapies to slow or prevent further degeneration and to promote neuronal repair are current goals in the management of PD The development and validation of diagnostic markers in symptom recognition and neuroimaging will aid in early diagnosis of PD Advances in neuroimaging and development of quantitative diagnostic biomarkers will also improve evaluation of potential neuroprotective therapies
  32. 32. References:- Cosgrove, G. Rees, Eskandar, Emad N., Shinobu, Leslie A. “Surgical Treatment of Parkinson Disease.” JAMA December 26, 2001;286:3056-3059. Dipiro, Joseph T., ed. Pharmacotherapy Fourth Edition. Stamford, Connecticut: Appleton & Lange, 1999. “Early Parkinson’s Disease: Dopamine Agonists Have Increasingly Important Role in Symptom Management.” Drug Ther Perspect 2001;17(17). Hermanowiez, Neal. “Management of Parkinson’s Disease.” Postgraduate Medicine 2001;110(6):15- 28 Korczyn, Amos D. “Hallucinations in Parkinson’s Disease.” Lancet 2001;358(9287):1031-1032.
  33. 33. Thank you