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PARKINSON’S
DISEASE
Prepared by
Swaliha C K
Assistant Professor
Senghundhar College of Pharmacy
Parkinson’s
Disease
Parkinson’s disease , is named after James
Parkinson who in 1817 wrote a classic
“shaking palsy”a disease for which the
reason is still unknown .
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 kinesia),
increased muscle tone (rigidity), tremor and impaired
postural reflexes
Parkinson’s disease is a chronic progressive degenerative
disorder of the CNS caused by an imbalance b/w
dopaminergic and cholinergic activity in the brain due to
degeneration of dopaminergic neurons resulting in depleted
level of dopamine in the brain leading to motor function
disorder and various other extrapyramidal symptoms
The famous internationally known boxer Mr.
Mohammed Ali suffered from this disease.
Occurs in the age group of 60s. Mostly men
are affected than women.
CLASSIFICATION
1.Primary /idiopathic parkinsonism
2. secondary/drug induced parkinsonism
1.Primary parkinsonism
•Cause is unknown
•Predominantly affecting individuals over60 years of age
•Over the years the dopaminergic neurons degenerate due to
H2O2 and free radicals such as superoxide and peroxynitrite
2.Secondary /drug induced parkinsonism
There is no degenaration as seen in above case but the decrease
in dopamine is drug induced
•Drugs that deplete the central stores of dopamine.eg
methyldopa, reserpine
•Drugs that antagonize D receptor .eg: phenothiazine,
butyrophenone
•Infections like viral encephalitis
•Toxins like 1-methyl 4-phenyl 1,2,3,6 tetrahydropyridine
(MPTP)
Etiology
• Heredity
• Antipsychotic drugs (or neuroleptic agents)
• Encephalitis infection in response to brain trauma,
tumors, hydrocephalus or ischaemia
• Arteriosclerosis
• Neurotoxins such as cyanide, manganese and
carbon monoxide
• Drugs like reserpine (hydropress), meyhyl dopa
(aldomet), haloperidol (haldol) and phenothiazine
(thorazine)
Pathophysiology
Antipsychotic drugs , encephalitis and other
causes
↓
Affects the substantia nigra
↓
Destuction of dopamine producing neurons
within the basal ganglia
↓
Reduces the amount of available straital
dopamine ( inhibitory effects )
There is increase in acetylcholine
(excitatory effects )
↓
Excitatory activity of Ach is inadequately
balanced
↓
Difficulty in controlling and initiating
voluntary movements
Clinical manifestations
In the beginning stages
•
•
•
•Mild tremor
•Slight limp
•Decreased arm swing
Later
•Shuffling, propulsive gait with arms flexed
Loss of postural reflexes
•Slight change in speech pattern
Classic clinical manifestations
1.Tremor
First sign affects hand writing
Non intentional, present at rest but usually not during
sleep
Movement of thumb across the palm gives a “pill
rolling” character
Tremor also seen in limbs, jaw, lips, lower facial
muscles and head
2. Rigidity
•
•
•
• Increased resistance to passive motion when the limbs
are moved through their range of motion
• Muscles feel stiff and required increased effort to
move
• Discomfort or pain may be percieved in muscle when
rigidity is severe
• “Cog wheel” rigidity refer to rachet – like rhythmic
contractions of the muscle that occur when the limbs
are passively stretched
3. Bradykinesia (akinesia)
•
•
•
•Slowness of active movement
•Difficulty in initiating movement
Often the most disabling symptom:
•interferes with ADK and predisposes patient to
complication related to constipation , circulatory
stasis, skin breakdown and related complications
of immobility .
4.Postural instability
•
•
•
•
i) Changes in gait
•Tendency to walk forward on the toes with small
shuffling steps
•Once initiated, movement may accelerate almost to
trot
•Festination may occur, which propels the patient
either forward or backward propulsively until falling
is inevitable.
ii) Changes in balance
•
•
•
•
•Stooped- over posture when erect
•Arms are semi flexed and do not swing with
walking
•Difficultyin maintaining balance and sitting
erect
•Cannot ‘right’ or brace self to prevent falling
,when balance is lost
Secondary manifestations
1)Facial appearance
•
•
•
•Expressionless
•Eyes store straight ahead
•Blinking is much less frequent than normal
2) Speech problems
•
•
•
•
•Low volume
•Monotone
•Difficulty with starting speech and word finding
3) Visual problems
• Blurred vision
• Impaired upward gaze
• Blepharospasm- involuntary prolonged closing
of the eyelids
4) Fine motor function
•
•
•
•
• Microphagia- handwriting progressively
decreases in size
• Decreased manual dexterity
• Clumsiness and decreased co-ordination
Decreased capacity to complete ADL.
• Freezing- sudden involuntary inability to initiate
movement can occur during movement or
inactivity
5) Autonomic disturbances
Constipation- hypomotility and prolonged
gastric emptying
Urinary frequency or hesitency
Orthoststic hypotension(dizziness, fainting and
syncope)
Dysphagia( neuro muscular in co-ordination )
Drooling( results from decreased swallowing )
Oily skin
Excessive perspiration
6)Cognitive / behavioral
•
•
•
•
•
•Depression
•Slowed responsiveness
•Memory deficit
•Visual-spacial deficit Dementia
DIAGNOSIS
•Physical examination
•Neurological examination
•Autopsy of brain to find lewy body
•Computed tomography scan (CT scan)
•Dopamine transporter imaging inspection test
MANAGEMENT
NON- PHARMACOLOGICAL
•Education
•Nutrition
•Psychiatric counseling
•Exercise
•Speech therapy
•Occupational therapy
Pharmacological management
 Dopamine agonist
 Anti- cholinergics
 Anti- histaminics
 MAO inhibitors
 COMT inhibitors
Dopamine agonist
•Levodopa
•Carbidopa
Anti-cholinergics
•Benztropine
•Trihexyphenidyl
Anti-histamines
•Diphenhydramine
•Promethazine
MAO- B inhibitors
•Selegeline
•Phenelzine
COMT inhibitors
•Entacapone
•Tolcapone
Parkinson's disease

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Parkinson's disease

  • 1. PARKINSON’S DISEASE Prepared by Swaliha C K Assistant Professor Senghundhar College of Pharmacy
  • 2. Parkinson’s Disease Parkinson’s disease , is named after James Parkinson who in 1817 wrote a classic “shaking palsy”a disease for which the reason is still unknown .
  • 3. 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 kinesia), increased muscle tone (rigidity), tremor and impaired postural reflexes
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  • 5. Parkinson’s disease is a chronic progressive degenerative disorder of the CNS caused by an imbalance b/w dopaminergic and cholinergic activity in the brain due to degeneration of dopaminergic neurons resulting in depleted level of dopamine in the brain leading to motor function disorder and various other extrapyramidal symptoms
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  • 7. The famous internationally known boxer Mr. Mohammed Ali suffered from this disease. Occurs in the age group of 60s. Mostly men are affected than women.
  • 8.
  • 9. CLASSIFICATION 1.Primary /idiopathic parkinsonism 2. secondary/drug induced parkinsonism 1.Primary parkinsonism •Cause is unknown •Predominantly affecting individuals over60 years of age •Over the years the dopaminergic neurons degenerate due to H2O2 and free radicals such as superoxide and peroxynitrite
  • 10. 2.Secondary /drug induced parkinsonism There is no degenaration as seen in above case but the decrease in dopamine is drug induced •Drugs that deplete the central stores of dopamine.eg methyldopa, reserpine •Drugs that antagonize D receptor .eg: phenothiazine, butyrophenone •Infections like viral encephalitis •Toxins like 1-methyl 4-phenyl 1,2,3,6 tetrahydropyridine (MPTP)
  • 11. Etiology • Heredity • Antipsychotic drugs (or neuroleptic agents) • Encephalitis infection in response to brain trauma, tumors, hydrocephalus or ischaemia • Arteriosclerosis • Neurotoxins such as cyanide, manganese and carbon monoxide • Drugs like reserpine (hydropress), meyhyl dopa (aldomet), haloperidol (haldol) and phenothiazine (thorazine)
  • 12. Pathophysiology Antipsychotic drugs , encephalitis and other causes ↓ Affects the substantia nigra ↓ Destuction of dopamine producing neurons within the basal ganglia ↓ Reduces the amount of available straital dopamine ( inhibitory effects )
  • 13. There is increase in acetylcholine (excitatory effects ) ↓ Excitatory activity of Ach is inadequately balanced ↓ Difficulty in controlling and initiating voluntary movements
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  • 15. Clinical manifestations In the beginning stages • • • •Mild tremor •Slight limp •Decreased arm swing Later •Shuffling, propulsive gait with arms flexed Loss of postural reflexes •Slight change in speech pattern
  • 16. Classic clinical manifestations 1.Tremor First sign affects hand writing Non intentional, present at rest but usually not during sleep Movement of thumb across the palm gives a “pill rolling” character Tremor also seen in limbs, jaw, lips, lower facial muscles and head
  • 17. 2. Rigidity • • • • Increased resistance to passive motion when the limbs are moved through their range of motion • Muscles feel stiff and required increased effort to move • Discomfort or pain may be percieved in muscle when rigidity is severe • “Cog wheel” rigidity refer to rachet – like rhythmic contractions of the muscle that occur when the limbs are passively stretched
  • 18. 3. Bradykinesia (akinesia) • • • •Slowness of active movement •Difficulty in initiating movement Often the most disabling symptom: •interferes with ADK and predisposes patient to complication related to constipation , circulatory stasis, skin breakdown and related complications of immobility .
  • 19. 4.Postural instability • • • • i) Changes in gait •Tendency to walk forward on the toes with small shuffling steps •Once initiated, movement may accelerate almost to trot •Festination may occur, which propels the patient either forward or backward propulsively until falling is inevitable.
  • 20. ii) Changes in balance • • • • •Stooped- over posture when erect •Arms are semi flexed and do not swing with walking •Difficultyin maintaining balance and sitting erect •Cannot ‘right’ or brace self to prevent falling ,when balance is lost
  • 21. Secondary manifestations 1)Facial appearance • • • •Expressionless •Eyes store straight ahead •Blinking is much less frequent than normal 2) Speech problems • • • • •Low volume •Monotone •Difficulty with starting speech and word finding
  • 22. 3) Visual problems • Blurred vision • Impaired upward gaze • Blepharospasm- involuntary prolonged closing of the eyelids
  • 23. 4) Fine motor function • • • • • Microphagia- handwriting progressively decreases in size • Decreased manual dexterity • Clumsiness and decreased co-ordination Decreased capacity to complete ADL. • Freezing- sudden involuntary inability to initiate movement can occur during movement or inactivity
  • 24. 5) Autonomic disturbances Constipation- hypomotility and prolonged gastric emptying Urinary frequency or hesitency Orthoststic hypotension(dizziness, fainting and syncope) Dysphagia( neuro muscular in co-ordination ) Drooling( results from decreased swallowing ) Oily skin Excessive perspiration
  • 25. 6)Cognitive / behavioral • • • • • •Depression •Slowed responsiveness •Memory deficit •Visual-spacial deficit Dementia
  • 26. DIAGNOSIS •Physical examination •Neurological examination •Autopsy of brain to find lewy body •Computed tomography scan (CT scan) •Dopamine transporter imaging inspection test
  • 29. Pharmacological management  Dopamine agonist  Anti- cholinergics  Anti- histaminics  MAO inhibitors  COMT inhibitors