Parkinson's disease is a neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra. Its characteristic motor symptoms include tremors, rigidity, bradykinesia, and impaired balance and coordination. The pathology involves the degeneration of neurons containing Lewy bodies, which are abnormal accumulations of the protein alpha-synuclein. While most cases are idiopathic, some familial cases are associated with genetic mutations. Treatment focuses on dopamine replacement therapy using levodopa or dopamine agonists to manage motor symptoms.

1. PARKINSON’S
DISEASE
BY-S.MODAK ,BPT FINAL YEAR(BMC)

2. INTRODUCTION
Parkinson’s disease was first described in England in 1817 by james
Parkinson.the condition was popularly known as shaking palsy derived
from latin word paralysis agitans,Recognised as an extrapyramidal
disorder by kinnier Wilson(1912).
➢Annual incidence :20 per 100000, Prevalence : 190 per 100000
➢Sex incidence : male : female – 3:2
➢Age of onset : 50 years upwards.incidence peaks in mid 70s then
declines.
➢Familial incidence occurs in 5%

3. DEFINATION
◦It is a slowly progressive
neurodegenerative disorder
(Depletion of dopaminergic
neurons in basal ganglia)
characterized by muscle
rigidity ,tremor at rest
,bradykinesia & gait
changes. In extreme cases, a
loss of physical movement
(Akinesia) seen.

4. ANATOMY OF BASAL GANGLIA

6. PATHOPHYSIOLOGY

8. PATHOLOGY of idiopathic Parkinson’s disease
❑DIRECT PATHWAY:- Corticostriatal fibers striatopallidal fibers palllidothalamic fibers thalamocortical fibers
❑INDIRECT PATHHWAY :- Corticostriatal fibers striatopallidal externum pallidosubthalamic subthalamic pallidointernus
➢Pallidothalamic fibers thalamocortical fibers
❖In case of parkinson’ s disease subtantia nigra & dopaminergic pathway degeneration occur so, mainly direct pathway
affected as well as indirect pathway affected.
❑The substantia nigra contains pigmented cells
(neuromelanin) which give it a characteristic
‘black’ appearance (macroscopic). These cells
Are lost in parkinson’s disease and the substantia
Nigra becomes pale.
Remaining cells contain atypical eosinophilic
inclusions in the cytoplasm – LEWY BODIES –
These lewy bodies are from due to abnormal
Accumulation of alpha synuclein (SNCA) In
Brain.

9. ETIOLOGY
➢The cause of Parkinson disease is idiopathic .Gene mutations have been identified in young
onset & familial cases (Alpha-synuclein gene, parkin gene ,Ubiquitin gene mutation , LRRK2)
➢Environmental toxins MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine),occasionally
pesticides.
➢Infections (post encephalitic/prion disease/HIV)
➢Drug induced (dopamine receptor blockers-antipsychotics/antiemetics , sodium valproate)
➢Smoking &coffee drinking have been associated with a lower risk of PD
❑MIMICS:-
✓Multiple system atrophy(MSA)
✓Progressive supranuclear palsy (PSP)
✓Corticobasal ganglionic degeneration (CBD)
✓Diffuse Lewy body disease (DLBD)

11. CLINICAL FEATURES
❑TREMOR :- It is an involuntary rhythmic oscillation around the joint . In case of parkinsonism, resting or static
tremor seen at a rate of 4-7 Hz. It is also called drum-beating tremor & ‘pill rolling’ movements (the thumb moving
rhythmically backward & forwards on the palm of the hand) seen.
❑RIGIDITY:-Defined as increased resistance to passive motion.
✓Cogwheel rigidity:- jerky,ratchet like resistance to passive movement and muscles alternately tense and relax.
✓Lead-pipe rigidity:- the muscular stiffness occurs because of increased muscle tone which is due to the removal of
inhibitory influence on gamma motor neurons . It affects both flexor & extensor muscle equally. So, the limbs
become more rigid like pillars.
❑SLOWNESS OF MOVEMENTS :- over the time,movements start slowing down (bradykinesia) & gradually , the
patient becomes unable to initiate the voluntary activity (akinesia)or the voluntary movements are reduced
(hypokinesia), it is because of hypertonicity of the muscles.
❑POVERTY OF MOVEMENTS :- because of absence of the automatic associate movements , the body becomes
statue like. The face becomes mask-like due to absence of appropriate expressions like blinking and smilling.

12. ❑CHANGE IN GAIT :- the gait becomes shuffling & festinant (small rapid steps to ‘keep up with’ the centre of
gravity) and the posture more flexed .
❑SPEECH & HANDWRITING PROBLEMS :- patient may speak very softly or sometimes rapidly .The words are
repeated many times. The speech becomes slurred and they hesitate to speak. And the handwriting reduces in size.
❑EMOTIONAL CHANGES :- the persons affected by Parkinson disease are often upset emotionally(depression occurs
in about 50%)
❑DEMENTIA :- in later stages of the disease some patients develop dementia.
❑Rising from a chair becomes laborious with progressive difficulty in initiating lower limb movement from a
stationary position.
❑Eye movements may be affected with loss of ocular convergence and upward gaze.
❑Excessive sweating and greasy skin (seborrhoea) can be troublesome.
❑AUTONOMIC FEATURES OCCUR :-postural hypotension,constipation.

13. DIAGNOSIS

14. TREATMENT

18. SURGICAL MANAGEMENT
❑THALAMOTOMY :- it is the destruction of small group of cells in thalamus.this surgery is done
to abolish tremors on the side of the body opposite to the surgery.
❑PALLIDOTOMY :-it is the surgical destruction of a group of cells in the internal globus pallidus.
these procedures are most effective in relieving dyskinesias &tremors.
❑DEEP BRAIN STIMULATION (DBS) SURGERY :- electrodes are inserted into the targeted brain
region using MRI and neuro-physiological mapping to ensure that they are implanted in the right
place . A device called an impulse generator or IPG(similar to a pacemaker) is implanted under
the collar bone to provide an electrical impulse to a part of the brain involved in motor function.
Those who undergo the surgery are given a controller , which allows them to check the battery
and turn the device on or off. An IPG battery lasts for about three to five years and is relatively
easy to replace under local anesthesia.

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