The document discusses Parkinson's disease, defining it as a chronic neurodegenerative disorder that affects the neurons of the basal ganglia and leads to loss of dopamine-producing brain cells. Some key causes include genetic mutations and environmental toxins. Clinically, it is characterized by tremors, rigidity, akinesia/bradykinesia, and postural instability. While there are no specific tests, investigations like CT/MRI are used to rule out other conditions. Treatment involves drug therapy like levodopa and dopamine agonists, as well as surgical options like deep brain stimulation.

1. PARKINSON’S DISEASE
Dr. K. MALATHI
MD SCHOLAR
DEPT. OF. KAYACHIKITSA
DR. NRS GOVERNMENT AYURVEDIC COLLEGE
VIJAYAWADA.

2. DEFINITION
It is a chronic nurodegenerative
disorder that which primarily effects
the nurons of the basal ganglion,
which leads to progressive
deterioration of motor function due
to loss of dopamine producing brain
cells – substantia nigra
Occurs in the age group of 60 years.
Affects the Men >women

3. CAUSES
 Idiopathic
Environmental toxins – MPTP(methyle phynyl
tetra hydropyridine) , Pesticides
Viral infections
Genetic factors – genetic mutations 1-2%
GBA, SNCA, LARK2, PARK2

4. Patho physiology
 Mainly basal ganglia – controls the movements
Dopamine – inhibitory nurotransmeter in the
basal ganglia
Acetylcholine – Excitatory nurotransmeter in the
basal ganglia
Metabolism of dopamine by MAO produce
hydrogen peroxide.
Glutathione normally breaks down the hydrogen
peroxide quickly.
Reduced Glutathoione leads to loss of protection
against free radicles leads to Cell damage.

5. Pathogenesis probably involves
apoptosis or necrosis of
dopaminergic neurons, results of
death of neurons
involvement of toxins due to
defective proteolysis, mitochondrial
dysfunction and oxidative stress
etc.,

6. There is depletion of pigmented
dopaminergic neurons in the sustantia nigra.

7. CLINICAL FEATURES
Cardinal features: TRAP
TREMORS
RIGIDITY
AKINESIA / BRADYKINASIA
POSTURAL INSTABILITY
 General features :
Masked face / expressionless face
Dysphagia
Hypophonia
Dysphonia
Assymetrical gait

8. Tremors
 Resting (4 – 6 Hz)
Postural ( 8-10 Hz)
Increases when activity
Aresting tremors in upperlimb being a common
presenting feature
Although Parkinsonian features are initially
unilater later in progressively bilateral

9. Rigidity
 Cog wheel type – mostly in
upperlimbsSuper imposed tremor,
felt as tightness stiffness of the
limb muscles
 Plastic /Lead pipe leg – stiffness of
the lower limb

10. Bradykinesia
 Slowed ability to start/ initiation
to continue the movement
Impaired ability to adjust body
position
Impaired fine movements

11. Postural disability
 Head bowed
Body bent forward
Back rigidity
Arms flexed
Thumbs turned into palms
Knees slightly flexed

12. Tests for Bradykinesia
 Finger tapping
Hand movements
Pronation supination
movements of the arms
Leg agility
Neurological examination :
 Muscle strength
 Hypomimia- loss of expression
 Cognitive impairment
 Sensation and intellectual ability
 Eye movement

13. Investigations
There no specific medical tests used to
diagnose the Parkinson’s disease
However CT, MRI and other blood tests used
to find out other possible conditions as similar
to Parkinson’s disease

14. Treatment
 Drug therapy
Surgical treatment
Speech therapy
Physio therapy
Nutrition planning

15. Pharmacological management
 Anti Cholinergics
Anti histamines
Dopaminergics
MAO inhibitor
Dopamine agonist's
EXAMPLES :
LEVODOPA
BROMOCRIPTINE
ROPINIROLE
CABERGOLINME
PERGOLIDE ETC

16. Surgical treatments
 TALAMOTOMY
DEEP BRAIN STIMULATION
PALLIDOTOMY
VECTOR MEDOIATED GENE THERAPY