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Presented by,
ved prakash panda
M. pharm (pharmacology)
Clinical Pharmacology & Pharmaco Therapeutics.
Parkinsonism &Alzheimer disease:
DEFINITION:
 Parkinsonism is a disorder caused by degeneration of basal
ganglia, causing impairment of motor nerves and disabling motor
functions. It is caused due to decreased activity of dopamine or
increase in the activity of acetylcholine in striatum present in the
basal ganglia.
 A disorder of central nervous system that affects movement, often
including tremors.
ETIOLOGY:
The decrease in dopamine levels is due to many reasons:
1. Ageing causes defective electron transfer in mitochondria, hence
parkinsonism mostly occurs in individual above 60yrs of age.
2. Genetic factors.
3. Production of free radicals during metabolism of
neurotransmitters. These free radicals damage the brain cells and
reduce dopamine levels.
4. Poisons and poisonous environment.
PHYSIOLOGY:
 Generally dopamine causes activation of direct pathway (D1
receptor) and inhibition of indirect pathway (D2receptor). This
results in excitation of cortex, leading to voluntary movements.
 In parkinsonism, where the dopamine gets depleted due to
destruction of dopaminergic neurons, the direct pathway gets
suppressed, while the indirect pathway gets over stimulated. This
leads to decreased excitatory outflow to motor cortex resulting in
the suppression of voluntary movement.
FACTORS:
 Demographic factors: Age (elders) ,Gender(men).
 Genetic factors: Family history, Onset of PD before 50yrs of age
in twin study.
 Life experiences: Head injury and trauma, Emotional stress,
personality.
 Dietary factors: Animal fat consumption.
 Infectious agents and disease: HIV, measles, mumps diphtheria,
rheumatic fever ,influenza.
 Environmental factors: Rural living, farming activity, well water
drinking, pesticide exposure,
PATHOPHYSIOLOGY:
 The dopaminergic neurons from substantia nigra pars compacta
acts on excitatory d1 receptors and causes excitation of the
stratum neurons in direct pathway. This excitation is neutralized
when dopaminergic neurons from substantia nigra pars compacta
acts on inhibitory d2 receptors and causes inhibition of striate
neurons in the indirect pathway.
 In direct pathways , the globus pallidus and the substantia
nigra are innervated via inhibitory GABAnergic neuron. Similarly
the neurotransmission from these two regions are carried to
thalamus by GABAnergic neuron .However the transmission of
neuron from thalamus to cortex is carried by excitatory
Glutaminergic neurons results in voluntary movements.
In indirect pathways the movement of transmission from striatum to
subtalamus is innervated by inhibitory GABAnergic neuron. But
transmission from subthalamus to globus pallidus medulla and
substantia nigra pa recticulata is by excitatory glutaminergic
neurons . Hence alteration in the innervation to globus pallidus and
substantia affects the neurotransmission in cortex which result in
suppression of voluntary movements.
DIAGNOSIS:
Acute effect:
 Shaking
 Rigidity
 Slowness of movement
 Difficult in walking.
Chronic effect :
 Dementia
 Depression
 Anxiety
ADVERSE EFFECTS:
 Dryness of mouth.
 Constipation.
 Urinary retention.
 Confusion.
 Restlessness.
 Hallucination.
 Cardiac arrhythmias.
 Marked hypotension.
TREATMENT:
 Pharmacological uses: Levodopa, Carbidopa, Entacapone,
Tolcapone, Amantadine, Procyclidine, Bromocriptine.
 Non pharmacological uses: Diet and Exercise.
 Intake of rich fiber food and high intake of water.
 Exercise improve motor activity
 Counseling
ALZHEIMER DISEASE:
‘Alzheimer disease is a neurological disorder in which the death of
brain cells causes memory loss and cognitive decline. A
neurodegenerative type of dementia, the disease starts mild and
gets progressively worse.
German psychiatrist
Described symptoms + pathology
Neuronal loss
Plaques
Tangles
ETIOLOGY:
 Risk factors:
 Hypertension.
 Increased age( above 65yrs).
 Increased cholesterol levels.
 Coronary artery disease.
 Diabetes.
Other factors: Genetics, Smoking and alcohol use, Down syndrome,
Mild cognitive impairments.
PATHOPHYSIOLOGY:
 Alzheimer’s disease is characterized by the loss of neurons and
synapses in the cerebral cortex and certain sub cortical regions.
 This loss results in gross atrophy of the affected regions ,
including degeneration in the temporal lobe and parietal lobe and
parts of frontal
cortex and cingulated gyrus.
DIAGNOSIS:
 Detailed patient history
 Information from family and friends
 Laboratory tests like:
 Rule out vit B12 and folate deficiency
 Rule out hypothyroidism with TFT tests
 Blood cell count , serum electrolyte and LFT
 Other diagnostic tests:
CT, PET or MRI scans may aid diagnosis.
The “Do-It-Yourself” Approach:
- Diet control
- Use of exercise
- Stress control
- Herbal remedies
THANK YOU…….

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Parkinsonism & Azheimers

  • 1. Presented by, ved prakash panda M. pharm (pharmacology) Clinical Pharmacology & Pharmaco Therapeutics. Parkinsonism &Alzheimer disease:
  • 2. DEFINITION:  Parkinsonism is a disorder caused by degeneration of basal ganglia, causing impairment of motor nerves and disabling motor functions. It is caused due to decreased activity of dopamine or increase in the activity of acetylcholine in striatum present in the basal ganglia.  A disorder of central nervous system that affects movement, often including tremors.
  • 3. ETIOLOGY: The decrease in dopamine levels is due to many reasons: 1. Ageing causes defective electron transfer in mitochondria, hence parkinsonism mostly occurs in individual above 60yrs of age. 2. Genetic factors. 3. Production of free radicals during metabolism of neurotransmitters. These free radicals damage the brain cells and reduce dopamine levels. 4. Poisons and poisonous environment.
  • 4. PHYSIOLOGY:  Generally dopamine causes activation of direct pathway (D1 receptor) and inhibition of indirect pathway (D2receptor). This results in excitation of cortex, leading to voluntary movements.  In parkinsonism, where the dopamine gets depleted due to destruction of dopaminergic neurons, the direct pathway gets suppressed, while the indirect pathway gets over stimulated. This leads to decreased excitatory outflow to motor cortex resulting in the suppression of voluntary movement.
  • 5. FACTORS:  Demographic factors: Age (elders) ,Gender(men).  Genetic factors: Family history, Onset of PD before 50yrs of age in twin study.  Life experiences: Head injury and trauma, Emotional stress, personality.  Dietary factors: Animal fat consumption.  Infectious agents and disease: HIV, measles, mumps diphtheria, rheumatic fever ,influenza.  Environmental factors: Rural living, farming activity, well water drinking, pesticide exposure,
  • 6.
  • 7. PATHOPHYSIOLOGY:  The dopaminergic neurons from substantia nigra pars compacta acts on excitatory d1 receptors and causes excitation of the stratum neurons in direct pathway. This excitation is neutralized when dopaminergic neurons from substantia nigra pars compacta acts on inhibitory d2 receptors and causes inhibition of striate neurons in the indirect pathway.  In direct pathways , the globus pallidus and the substantia nigra are innervated via inhibitory GABAnergic neuron. Similarly the neurotransmission from these two regions are carried to thalamus by GABAnergic neuron .However the transmission of neuron from thalamus to cortex is carried by excitatory
  • 8. Glutaminergic neurons results in voluntary movements. In indirect pathways the movement of transmission from striatum to subtalamus is innervated by inhibitory GABAnergic neuron. But transmission from subthalamus to globus pallidus medulla and substantia nigra pa recticulata is by excitatory glutaminergic neurons . Hence alteration in the innervation to globus pallidus and substantia affects the neurotransmission in cortex which result in suppression of voluntary movements.
  • 9.
  • 10. DIAGNOSIS: Acute effect:  Shaking  Rigidity  Slowness of movement  Difficult in walking. Chronic effect :  Dementia  Depression  Anxiety
  • 11. ADVERSE EFFECTS:  Dryness of mouth.  Constipation.  Urinary retention.  Confusion.  Restlessness.  Hallucination.  Cardiac arrhythmias.  Marked hypotension.
  • 12. TREATMENT:  Pharmacological uses: Levodopa, Carbidopa, Entacapone, Tolcapone, Amantadine, Procyclidine, Bromocriptine.  Non pharmacological uses: Diet and Exercise.  Intake of rich fiber food and high intake of water.  Exercise improve motor activity  Counseling
  • 13. ALZHEIMER DISEASE: ‘Alzheimer disease is a neurological disorder in which the death of brain cells causes memory loss and cognitive decline. A neurodegenerative type of dementia, the disease starts mild and gets progressively worse.
  • 14. German psychiatrist Described symptoms + pathology Neuronal loss Plaques Tangles
  • 15. ETIOLOGY:  Risk factors:  Hypertension.  Increased age( above 65yrs).  Increased cholesterol levels.  Coronary artery disease.  Diabetes. Other factors: Genetics, Smoking and alcohol use, Down syndrome, Mild cognitive impairments.
  • 16.
  • 17.
  • 18. PATHOPHYSIOLOGY:  Alzheimer’s disease is characterized by the loss of neurons and synapses in the cerebral cortex and certain sub cortical regions.  This loss results in gross atrophy of the affected regions , including degeneration in the temporal lobe and parietal lobe and parts of frontal cortex and cingulated gyrus.
  • 19. DIAGNOSIS:  Detailed patient history  Information from family and friends  Laboratory tests like:  Rule out vit B12 and folate deficiency  Rule out hypothyroidism with TFT tests  Blood cell count , serum electrolyte and LFT  Other diagnostic tests: CT, PET or MRI scans may aid diagnosis.
  • 20.
  • 21. The “Do-It-Yourself” Approach: - Diet control - Use of exercise - Stress control - Herbal remedies