Prakash park

Prakash Mahala
Prakash Mahalalecturer (nursing) à P.G.HIHT Deemed university dehradun
Parkinson’s
 Disease
    BY:- PRAKASH MAHALA
         M.SC.NURSING 1STYEAR
Introduction:-

 Dr. James Parkinson (1755-1828)

     “involuntary tremulous motion”
     “shaking palsy”

     London home
The disease was first
described in 1817 by a British
physician
named James Parkinson

He wrote "An Essay on
Shaking Palsy"
 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
 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
Definition :-

 Parkinson's 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.
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
Type :-

 There are three types of Parkinson's disease
  and they are grouped by age of onset:
 Adult-Onset Parkinson's Disease - This is the
  most common type of Parkinson's 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
  70's and 80's.
 Young-Onset Parkinson's Disease - The age
  of onset is between 21-40 years old. Though
  the incidence of Young-Onset Parkinson's
  Disease is very high in Japan (approximately
  40% of cases diagnosed with Parkinson's
  disease).

 Juvenile Parkinson's Disease - The age of
  onset is before the age of 21. The incidence of
  Juvenile Parkinson's Disease is very rare.
STAGES OF
PARKINSON’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
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)
   Head trauma
   Encephalitis has been clearly associated with
    parkinsonism.
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.
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.
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.
Prakash park
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
 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
 Feelings of anxiety, depression and loneliness.

 Excessive salivation (hypersalivation) and
  excessive sweating

 Constipation

 Soft, whispery voice (hypophonia)

 Slow response to questions (bradyphrenia)
Prakash park
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
COMT = catechol-O-methyltransferase; MAO-B = monoamine oxidase B
 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
 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.
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
 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 Parkinson's 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 isn't beneficial for people who don't
    respond to carbidopa-levodopa. And the device isn't for people
    who already have serious difficulty with thinking and memory
    because it may make those symptoms worse.
 Picture of electrode in sub-thalemic
  nucleus
Sources http://www.themedicaldirectory.org/essays/parkinsons
Nursing management :-
 Nursing interventions for each of the
  symptoms of Parkinson's disease, muscle
  rigidity, bradykinesia, tremors at rest and
  postural reflex abnormalities, are designed to
  increase the patient's quality of life by
  minimizing symptoms.
 Nurses are responsible for planning patient
  medication schedules to maximize drug
  effectiveness.
 Constipation is addressed by increasing the
  patient's fibre and fluid intake and by
  increasing the patient's 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.
 Dietary implications include a low-protein
regimen for the patient during the day, eliminating
foods high in Vitamin B6, high caloric foods, and
soft-solid foods offered at frequent feedings.
COMPLICATIONS:-

 Motor fluctuations
 Dyskinesis
 Posture, gait, falling
 Neuropsychiatric problems
 Sleep disorders
 Sensory phenomena
 Dysautonomias
 Speech disturbances
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
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.
Thank you
1 sur 35

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Prakash park

  • 1. Parkinson’s Disease BY:- PRAKASH MAHALA M.SC.NURSING 1STYEAR
  • 2. Introduction:-  Dr. James Parkinson (1755-1828)  “involuntary tremulous motion”  “shaking palsy”  London home
  • 3. The disease was first described in 1817 by a British physician named James Parkinson He wrote "An Essay on Shaking Palsy"
  • 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.  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. Definition :-  Parkinson's 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. 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. Type :-  There are three types of Parkinson's disease and they are grouped by age of onset:  Adult-Onset Parkinson's Disease - This is the most common type of Parkinson's 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 70's and 80's.
  • 9.  Young-Onset Parkinson's Disease - The age of onset is between 21-40 years old. Though the incidence of Young-Onset Parkinson's Disease is very high in Japan (approximately 40% of cases diagnosed with Parkinson's disease).  Juvenile Parkinson's Disease - The age of onset is before the age of 21. The incidence of Juvenile Parkinson's Disease is very rare.
  • 10. STAGES OF PARKINSON’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. 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. Head trauma  Encephalitis has been clearly associated with parkinsonism.
  • 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. 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. 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.
  • 17. 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
  • 18.  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
  • 19.  Feelings of anxiety, depression and loneliness.  Excessive salivation (hypersalivation) and excessive sweating  Constipation  Soft, whispery voice (hypophonia)  Slow response to questions (bradyphrenia)
  • 21. 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
  • 22. COMT = catechol-O-methyltransferase; MAO-B = monoamine oxidase B
  • 23.  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
  • 24.  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.
  • 25. 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
  • 26.  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 Parkinson's 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 isn't beneficial for people who don't respond to carbidopa-levodopa. And the device isn't for people who already have serious difficulty with thinking and memory because it may make those symptoms worse.
  • 27.  Picture of electrode in sub-thalemic nucleus
  • 29. Nursing management :-  Nursing interventions for each of the symptoms of Parkinson's disease, muscle rigidity, bradykinesia, tremors at rest and postural reflex abnormalities, are designed to increase the patient's quality of life by minimizing symptoms.  Nurses are responsible for planning patient medication schedules to maximize drug effectiveness.
  • 30.  Constipation is addressed by increasing the patient's fibre and fluid intake and by increasing the patient's 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.
  • 31.  Dietary implications include a low-protein regimen for the patient during the day, eliminating foods high in Vitamin B6, high caloric foods, and soft-solid foods offered at frequent feedings.
  • 32. COMPLICATIONS:-  Motor fluctuations  Dyskinesis  Posture, gait, falling  Neuropsychiatric problems  Sleep disorders  Sensory phenomena  Dysautonomias  Speech disturbances
  • 33. 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
  • 34. 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.