Parkinson's disease is a neurodegenerative disorder that results from the loss of dopamine-producing neurons in the substantia nigra region of the brain. This leads to decreased dopamine levels in the basal ganglia and symptoms like tremors, rigidity, slowed movement, and impaired balance. The disease was first described in 1817 and is diagnosed based on the presence of two of the four main motor symptoms. Treatment options include dopamine replacement medications, surgery like deep brain stimulation to regulate motor circuits, and experimental therapies involving fetal or stem cell transplants.

1. Parkinson’s Disease
International school of medicine
neurology
Mini alekya
Group 4

2. Neurological Basis
• “Neurodegenerative Disease” : caused by degeneration
(dysfunction and death) of neurons within the brain
(nigrastriatal pathway of the basal ganglia) Parkinson’s
disease affects the nerve cells in the brain that produce
dopamine. Parkinson’s disease affects the nerve cells in
the brain that produce dopamine.
• NORMAL BRAIN FUNCTION – Basal Ganglia
• Cells in substantia nigra produce/release dopamine
• Dopamine released by SN neurons lands on neurons of
other brain centers, controlling their firing
• Main targets are caudate nucleus and putamen (striatum)
• This basal ganglia pathway is involved in regulation of
movement

4. Neurological Basis
• PARKINSON’S BRAIN FUNCTION–Basal
Ganglia
• Cells of substantia nigra degenerate
• These cells can no longer produce adequate amounts of
dopamine
• Neurons of striatum, etc. are no longer well regulated,
thus do not behave in normal manner
• Results in loss of control of movements – leads to
symptoms characteristic of Parkinson’s disease

5. • The term parkinsonism is used for a
motor syndrome whose main symptoms
are tremor at rest, stiffness, slowing of
movement and postural instability.
Parkinsonian syndromes can be divided
into four subtypes according to their origin:
• primary or idiopathic
• secondary or acquired
• hereditary parkinsonism, and
• Parkinson plus syndromes or multiple
system degeneration

6. CORE BIOCHEMICAL
PATHOLOGY
• IS DECREASED DOPAMINE
NEUROTRANSMISSION IN THE BASAL
GANGLIA. MOST PARKINSON SYNDROMES
HAVE DEGENERATION OF THE
NIGROSTRIATAL DOPAMINE SYSTEM WITH
MARKED LOSS OF STRIATAL DOPAMINE. IN
SOME – STRIATAL DEGENERATION WITH
LOSS OF DOPAMINE RECEPTORS OCCURS.

7. DRUG INDUCED PARKINSON
RESULTS FROM:
• BLOCKAGE OF DOPAMINE RECEPTORS OR
• DEPLETION OF DOPAMINE STORAGE,
DECREASED DOPAMINERGIC ACTIVITY IN THE
STRIATUM LEADS TO DISINHIBITION OF THE
SUBTHALMIC NUCLEUS AND THE MEDIAL
GLOBUS PALLIDUS, THE PROMINENT EFFERENT
NUCLEUS OF THE BASAL GANGLIA.
UNDERSTANDING HAS LED TO DOPAMINE
REPLACEMENT, SURGICAL TREATMENT

8. Characteristic Symptoms
• MOTOR
– tremor
– bradykinesia
– rigidity/freezing in
place
– lack of facial
expression
– postural instability
– stooped, shuffling gait
• NONMOTOR
– diminished sense of
smell
– low voice volume
– foot cramps
– sleep disturbance
– depression
– constipation
– drooling

9. 1817 – DESCRIBED BY
JAMES PARKINSON
SIX CARDINAL FEATURES
• REST TREMOR
• RIGIDITY
• FLEXED POSTURE
• BRADYKINESIA – HYPOKINESIA
• LOSS OF POSTURAL REFLEXES
• FREEZING PHENOMENON
TO DIAGNOSE: TWO OF ABOVE, WITH AT
LEAST ONE BEING REST TREMOR OR
BRADYKINESIA

10. Diagnosis
• Diagnosing Parkinson's Disease
• There's no precise test for Parkinson's disease. This article describes how
doctors diagnose the condition.
• PET Scan
• For patients with Parkinson's disease (PD), a PET scan is used to assess
activity and function of brain regions involved in movement.
• CT Scan
• CT, or computed tomography, uses X-rays and computers to produce
images of inside the body including the brain. This test is used to look for
signs of disease like Parkinson's in the body .
• MRI
• MRI, or magnetic resonance imaging, is a test that produces very clear
pictures, or images, of the human body without the use of X-rays. Instead,
MRI uses a large magnet, radio waves, and a computer to produce these
images

12. • The central sulcus is more posteriorly on
more cranial images.
•

13. TREATMENT OF
PARKINSON DISEASE
• MEDICAL
– DOPAMINERGIC AGENTS
– ANTI-CHOLINERGICS;
etc.
• SURGICAL
– ABLATIVE
– RESTORATIVE
– D.B.S.
• PHYSICAL THERAPIES
– P.T.
– O.T.
– SPEECH
– OMT, BIOFEEDBACK
– EXERCISE Rx, TAI-CHI
• PSYCHOTHERAPIES
– COUNSELLING
– SOCIAL WORK
– MEDS., etc.

14. Conventional Treatments:
Medication
• LEVODOPA (L-DOPA)
• precursor to dopamine, converted to dopamine by
nerve cells in the brain
• Treatment with dopamine not possible, because
dopamine can’t cross blood-brain barrier
• Generally combined with carbidopa (Sinemet) –
helps levodopa get to the brain + reduces some
side effects
• Extended use often produces dyskinesias –
uncontrolled movements (writhing, twitching,
shaking) among other minor side effects

15. Conventional Treatments:
Medication
• DOPAMINE AGONISTS
• not changed into dopamine, but rather act LIKE
dopamine at brain synapses where dopamine is
usually present (nigrostriatal pathways in
Parkinson’s patients)
• Used both as adjuncts to L-Dopa therapy and in
younger Parkinson’s disease patients
• Side effects similar to levodopa, but less likely to
develop involuntary movements, more likely to
cause hallucinations

16. Conventional Treatments:
Medication
• MAO Inhibitors (Selegiline)
• COMT Inhibitors
• Anticholinergics

17. Conventional Treatments:
Surgery
• Thalamotomy
• Involves destruction of small amounts of tissue in
the thalamus—major center for relaying
messages/transmitting sensations
• Can cause slurred speech and lack of coordination
• Pallidotomy
• electric current used to destroy small amount of
tissue in the pallidum (globus pallidus)
• May improve tremors, rigidity by interrupting
pathway between globus pallidus and thalamus

18. Conventional Treatments:
Surgery
• Deep Brain
Stimulation
• implant device,
pacemaker-like unit
transmits impulses to
electrodes placed in
subthalamic nucleus
• Produces same effects
of lesion surgeries, but
can be turned on and
off

19. Experimental Treatment:
Surgery
• Fetal Cell Transplant Therapy
• stem cells obtained via aborted fetus, grown in culture,
transplanted into Parkinson’s patient at nigrostriatal pathway
• New cells establish connections and “replace” cells originally
lost, these cells function normally and even produce
dopamine
• Autologous “Self” Transplant
• analagous to fetal cell transplant, except that precursor
nerve cells are taken from patient and coaxed to produce
dopamine, then implanted back into original patient
• Reduces threat of autoimmune response and reduced
“controversial baggage” associated with FCT therapy