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Parkinson’s Disease
 Contents
 Introduction
 Definition
 Signs and Symptoms
 Etiology(causes)
 Diagnosis and treatment
 Conclusion
3
Parkinson’s
Disease
4
Introduction
 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
5
Definition
 It is a chronic degenerative disorder that primarily affects the neurons
of the basal ganglia.
 It is a syndrome that consists of slowing down in the initiation and
execution of movement (brady kinesis)
 Increased muscle tone (rigidity)
 Tremor and impaired postural reflexes.
 The famous internationally known boxer
Mr. Mohammed Ali suffered from this
Disease.
6
Symptoms
 There are 4 major symptoms for Parkinson Disease, They are:-
1. Rigidity – muscles are tensed and contracted.
2. Resting tremor – trembling which is most obvious when the patient
is at rest or when stressed.
3. Bradykinesia – slowness in initiating movement.
4. Loss of postural reflexes or instability – poor balance and
coordination.
7
Non-Motor Symptoms
 -Non-motor symptoms includes Anxiety disorders such as:-
 depression,
 sleep disturbances,
 orthostatic hypotension(also called postural hypotension — is a form of low
blood pressure that happens when you stand up from sitting or lying down).
 olfaction(smelling) dysfunction
 dysphagia(fail to produce and understand language)
 sialorrhoea(excess saliva production),
 dementia(memory declining)
 psychosis(memory disorder results in loss with external contact)
 and visual hallucinations(person see what does not really exist there).
8
Causes(Aetiology)
Degradation of dopaminergic neuron.
Free radicals.
Neurotoxin - MPTP
 Genetic factors.
9
Degradation of Dopaminergic Neuron/Free Radicals
 Degradation of Dopaminergic Neuron:-
 Substantia nigra pars compacta(pars compacta is the portion
of substantia nigra lies in mid brain region of our brain).
 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.
 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 10
Neurotoxin-MPTP/Genetic Factors
 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 and hence lead to cell death
via energy deficit.
 Genetic Factors:-
-Mutation of SNCA genes in chromosome 4.
-2 types of alterations occurs:-
1-Alanine is replaced with threonine.
2-Cause alpha-synuclein to misfold.
1-SNCA genes is inappropriately
duplicated or triplicated.
2-Extra copies of the gene lead to an
excess of alphasynuclein
Aggregate (Lewy bodies) and attract
other protein.
• Clog neuron and impair the function of
neuron
11
Diagnosis and Treatment
 Diagnosis:-
 Neurological examination
 Autopsy of brain to find lewy bodies (trademark characteristic)
 Treatment:-
 Medications
 Diet
 Exercise, physical and speech therapy
 Surgery which includes:-
 Cryothalamotomy
 Pallidotomy
 Deep brain stimulation
12
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(progress of disease): normal life expectancy for
treated patients.
13
References
 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.newsmedical.net/health/Parkinsons-Disease-
Pathophysiology.aspx. [Accessed on 1st March 2013].
 Dr. Ananya Mandal. (2013). Parkinson’s disease Prognosis. [Online]. Available
from: http://www.newsmedical.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].
 Mayo Clinic. Parkinson’s Disease: Risk Factors. [Online]. 14

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Parkinsons Disease-Decrease in neurotransmitter secretions.

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  • 3. Parkinson’s Disease  Contents  Introduction  Definition  Signs and Symptoms  Etiology(causes)  Diagnosis and treatment  Conclusion 3
  • 5. Introduction  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 5
  • 6. Definition  It is a chronic degenerative disorder that primarily affects the neurons of the basal ganglia.  It is a syndrome that consists of slowing down in the initiation and execution of movement (brady kinesis)  Increased muscle tone (rigidity)  Tremor and impaired postural reflexes.  The famous internationally known boxer Mr. Mohammed Ali suffered from this Disease. 6
  • 7. Symptoms  There are 4 major symptoms for Parkinson Disease, They are:- 1. Rigidity – muscles are tensed and contracted. 2. Resting tremor – trembling which is most obvious when the patient is at rest or when stressed. 3. Bradykinesia – slowness in initiating movement. 4. Loss of postural reflexes or instability – poor balance and coordination. 7
  • 8. Non-Motor Symptoms  -Non-motor symptoms includes Anxiety disorders such as:-  depression,  sleep disturbances,  orthostatic hypotension(also called postural hypotension — is a form of low blood pressure that happens when you stand up from sitting or lying down).  olfaction(smelling) dysfunction  dysphagia(fail to produce and understand language)  sialorrhoea(excess saliva production),  dementia(memory declining)  psychosis(memory disorder results in loss with external contact)  and visual hallucinations(person see what does not really exist there). 8
  • 9. Causes(Aetiology) Degradation of dopaminergic neuron. Free radicals. Neurotoxin - MPTP  Genetic factors. 9
  • 10. Degradation of Dopaminergic Neuron/Free Radicals  Degradation of Dopaminergic Neuron:-  Substantia nigra pars compacta(pars compacta is the portion of substantia nigra lies in mid brain region of our brain).  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.  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 10
  • 11. Neurotoxin-MPTP/Genetic Factors  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 and hence lead to cell death via energy deficit.  Genetic Factors:- -Mutation of SNCA genes in chromosome 4. -2 types of alterations occurs:- 1-Alanine is replaced with threonine. 2-Cause alpha-synuclein to misfold. 1-SNCA genes is inappropriately duplicated or triplicated. 2-Extra copies of the gene lead to an excess of alphasynuclein Aggregate (Lewy bodies) and attract other protein. • Clog neuron and impair the function of neuron 11
  • 12. Diagnosis and Treatment  Diagnosis:-  Neurological examination  Autopsy of brain to find lewy bodies (trademark characteristic)  Treatment:-  Medications  Diet  Exercise, physical and speech therapy  Surgery which includes:-  Cryothalamotomy  Pallidotomy  Deep brain stimulation 12
  • 13. 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(progress of disease): normal life expectancy for treated patients. 13
  • 14. References  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.newsmedical.net/health/Parkinsons-Disease- Pathophysiology.aspx. [Accessed on 1st March 2013].  Dr. Ananya Mandal. (2013). Parkinson’s disease Prognosis. [Online]. Available from: http://www.newsmedical.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].  Mayo Clinic. Parkinson’s Disease: Risk Factors. [Online]. 14