This document provides an overview of Parkinson's disease including: - It is a progressive neurodegenerative disorder caused by loss of dopaminergic neurons. - There are three main types: primary, secondary, and Parkinsonism plus syndromes. - Etiology includes both genetic and environmental factors. - Secondary Parkinsonism has many potential causes including certain medications, infections, toxins, and other neurodegenerative conditions. - Pathology involves degeneration in the substantia nigra leading to dopamine depletion in the striatum.

1. CLINICAL NEUROLOGY
ASSIGNMENT
SUBMMITED BY:-
AMITESH NAWAL BIHARI
Physio Intern
Batch July 2021/001

2. Parkinson’s

3. Parkinson’s Disease
A progressive neurodegenerative disorder
characterized by the loss of dopaminergic
neurons in the substantia nigra of the brain.
The term Parkinsonism is used to refer to a
group of disorders that produce
abnormalities of basal ganglia function.
These are of three types:-
1. Primary Parkinsonism
2. Secondary Parkinsonism
3. Parkinsonism Plus Syndrome
Primary Parkinsonism is the most common
cause affecting approx 78% of pts.
Secondary parkinsonism results from a
number of different causes.
Parkinsonism plus syndromes refer to those
conditions with symptoms of multiple
system degeneration.

4. ETIOLOGY
Parkinsonian symptoms can arise from
either the neuropathological condition
PD (idiopathic PD) or other forms of
Parkinsonism .
For neuropathological PD, 90% of cases
are sporadic .
10% are of genetic origin – 6 different
gene mutations have been identified –
the Parkin genes .
Genetic forms of PD are seen more
frequently in young onset PD.
A combination of environmental factors
or toxins, genetic susceptibility, and the
aging process may account for many of
the sporadic cases .

5. SECONDARY PARKINSONS
Can be caused by :
1.Medications – antipsychotics & antiemetics,
lithium, reserpine, aldomet
2.Sequelae of CNS infection – Prion Diseases,
Jakob Creuzfeldt, Subacute sclerosing
panencephalitis (SSPE), HIV, post encephalitic
3.Toxin Exposure – Manganese, Rotenone,
Paraquat
4.Vascular Metabolic Disorders – Binswanger’s
Disease
5.Drug Induced – MPTP
6.Certain neurodegenerative conditions may also
exhibit Parkinsonian features, these are called
the Parkinsons Plus Syndromes – progressive
supranuclear palsy, Lewy Body Dementia
7.Trauma – Pugilistic encephalopathy

6. PATHOLOGY
Basal ganglia:
Group of nuclei in the brain situated at the base of the
forebrain (striatum[caudate & putamen], globus pallidus,
substantia nigra [SN], subthalamic nucleus).
Associated with voluntary motor control, procedural
learning, eye movements, cognitive and emotional
functions.
The main input structure in BG is striatum.
Input is received from all parts of cerebral cortex via
corticostriate projection & also from substancia nigra.
Output is channeled via globus pallidus & SN to thalamus
and back to cortex, completing the loop.
Direct pathway facilitates BG output to thalamus &
cortex.
Indirect pathway provides disinhibition to subthalamic
nuclei & thus suppression of some movements.

7. PATHOPHYSIOLOGY
Pathological hallmark of PD :
degeneration of dopaminergic
neurons in the substantia nigra
compacta, resulting in depletion of
striatal dopamine.
This neurotransmitter regulates
excitatory & inhibitory outflow from
the basal ganglia.
Loss of dopamine results in overactive
indirect pathway leading to akinesia &
rigidity.
Underactive direct pathway leads to
bradykinesia.
Some of the dopaminergic neurons
survive, and these are found to
contain Lewy Bodies.

8. Pathophysiology of Parkinsons
Lewy Bodies are eosinophilic
intracytoplasmic inclusions,
composed of numerous
proteins .
Protein accumulation plays a
prominent role in the
pathogenesis of both
sporadic & familial forms of
PD .
Lewy bodies may actually
be cytoprotective .

9. Six Cardinal Features
1. Tremor at rest
2. Rigidity
3. Bradykinesia
4. Loss of postural reflexes
5. Flexed Posture
6. Freezing (Motor Block)
Diagnostic Criteria :
Definite Parkinsons : at least two of these
features must be present, one of them being # 1
or # 2
Probable : Feature # 1 or feature # 2 is present
Possible : at least two of features # 3 – 6 must be
present

10. Stages of PD
(Modified Hoehn & Yahr Scale)
Stage 0 No signs of disease
Stage 1 Unilateral disease
Stage 1.5 Unilateral disease plus axial involvement
Stage 2 Bilateral disease, without impaired balance
Stage 2.5 Bilateral disease, with impaired balance
Stage 3 Mild to moderate bilateral disease, some postural
instability; physically dependent
Stage 4 Severe disability; still able to walk or stand unassisted
Stage 5 Wheelchair-bound or bedridden

11. Diagnostic Testing
There are no clinical tests widely available
to definitively make the diagnosis,
however, if confirmation of the clinical
diagnosis is desired, order serial 6 – fluoro
L dopa PET scans which will demonstrate a
gradual decline in uptake in the putamen &
caudate in the Parkinsons patient
Alternative Imaging Study - Serial Beta CIT
SPECT imaging revealing gradual loss of
function in the striatum
On the right, see the PET scan of a patient
who underwent implantation of fetal tissue
into the right putamen - note the recovery
of function in the right putamen and the
progressive loss of function in the left
putamen

12. MRI Appearance in
Parkinsons Disease
Standard MRI studies in Parkinsons
are normal.
If warranted, consider High Field
Strength 1.5 Tesla T2 weighted
Brain MRI.
Typical Appearance in Parkinsons :
wider area of lucency will be noted
in the subthalamic nucleus that is
probably indicative of increased
accumulation of iron – iron
deposition occurs when there is a
loss of connectivity to the cortex

13. Early Non - Specific
Generalized stiffness
Pain or Paresthesias of the limbs – in
particular, shoulder pain
Constipation
Low Uric Acid Levels
Sleeplessness
Reduction in volume of the voice
Loss of sense of smell
Seborrheic Dermatitis
These symptoms precede onset of the
motor symptoms of Parkinsons
(A Retrospective Study of Early
Symptoms of Parkinsons Disease,
Przuntek, 1992)
 Problems with fine motor skills
 Decreased sense of smell
 Loss of appetite
 Tremor occurring with anxiety
 Decreased arm swing on one side – a
principal finding in Parkinsons is
asymmetry in neurological findings
 Decreased emotional expression
 Personality changes, especially
introversion & inflexibility
Early Specific
Signs of Parkinsons

14. Neuropsychiatric Disorders in
Parkinsons Disease
• Depression
• Anxiety, including panic attacks
• Cognitive Dysfunction
• Dementia
• Psychosis
• Confusion or delirium
• Apathy

15. Treatment
No cure currently exists
Treatment does not stop the progression of the disease
Offers symptomatic relief
Can temporarily restore function
Can enhance Quality Of Life
Each individual responds to drugs differently

16. Medications
1. Levodopa:-
Converted to dopamine in the bone, which is responsible for transmitting signals in the brain allowing for normal
movements
Often combined with Carbidopa (Sinemet), which ↑ the amount of Levodopa that goes to the brain.
2. COMT inhibitors:-
Blocks the action of catechol-O-methyltransferase, an enzyme that breaks down dopamine.
Entacapone (Comtan) and Tolcapone (Tasmar).
3. Dopamine agonists:-
Act like dopamine within the brain
Bromocriptine (Parlodel), Pramipexole (Mirapex), Ropinirole (Requip), and Apomorphine (Apokyn).
4. Amantadine:-
Unknown mechanism; may ↑ brain’s response to dopamine or releases stored dopamine
Amantadine (Symmetrel).
5. Anticholinergics:-
Exert a relaxing effect on the body
Benztropine Mesylate (Congetin), Procyclidine (Kemadrin), Biperiden (Akineton), and Trihexyphenidyl.
6. Selegiline:-
Unknown mechanism
Appears to inhibit the breakdown of dopamine
Usually added to a patient’s therapy when effectiveness of Levodopa is ↓
Selegiline (Zalapar, Eldepyrl, Emsam)

17. Surgery
Deep Brain Stimulation
Brain pacemaker, sends electrical
impulses to brain to stimulate the
subthalamic nucleus.
Improves motor functions and
reduce motor complications.
Complications include: brain
hemorrhage, seizures, death.
Pallidotomy is no longer performed
in the management of Parkinsons – it
is not as effective as Deep Brain
Stimulation (DBS)

18. Physiotherapy Management
Aims of Physiotherapy:
1. Maintain and improve levels of function and independence, which will help to
improve a person’s quality of life
2. Use exercise and movement strategies to improve mobility
3. Correct and improve abnormal movement patterns and posture, where
possible
4. Maximise muscle strength and joint flexibility
5. Correct and improve posture and balance, and minimise risks of falls
6. Maintain a good breathing pattern and effective cough
7. Educate the person with Parkinson’s and their carer or family members
8. Enhance the effects of drug therapy

19. MOTOR LEARNING program
• Practice Improves learning & performance in early
stages
• Large no. of repetitions to develop procedural skills
• Avoid long & complex movement sequences
• Avoid dual tasking
• Modify environment to reduce interference of task
• Focus of Attention to the task
• Use of structured instructional sets
• Repetitive drill like practise in advanced disease
• Use of visual cues like floor markings, laser device,
visual targets.
• Rhythmic auditory stimulation like the use of
metronome beat,or a steady beat or auditory cues
• Multisensory cues ( visual + auditory).

20. RELAXATION EXERCISES
Gentle rocking
Slow rhythmic, rotational
movements of extremities & trunk
Rhythmic initiation technique of
PNF
Diaphragmatic breathing during
exercise
Progressive relaxation technique
Gentle yoga
Tai chi
Stress management techniques
Active and passive ROM ex. 2-3
tmes a day
Focus on strengthening weak &
elongated extensor ms, and
elongating shortened tight
flexor ms
PNF (D1/D2 patterns, contract
relax)
Stretching techniques with
mobilisation
Avoid ballistic stretches
Passive positioning ( prone
lying)
FLEXIBILITY EXERCISES

21. STRENGTH TRAINING
Resistive training
Isokinetic training
Functional training activities
Pool exs.

22. FUNCTIONAL TRAINING
• Bed mobility
• Side lying rolling
• Transition to sitting
• Pelvic tilts
• Weight shifts in sitting
• Trunk rotations in sitting
• Bilateral PNF patterns in sitting
• Transition to stand
• Weight shifts in standing
• Stepping activity
• Standing wall push ups
• Quadruped creeping
• Quadruped to kneeling to half kneeling to standing
• Use of massage, facial PNF, stretch, verbal cueing, mirror to facilitate facial movements

23. BALANCE TRAINING
a) Focus on center of mass (COM) and limits of
stability(LOS) control training.
b) Improve posture in sitting, standing& dynamic
movement tasks
c) practice working on expanding the limits of
stability in sitting & standing
d) Use of verbal, tactile or proprioceptive cues to
facilitate proper posture and safety awareness
e) Use of standing platform training device
f) Practice of dynamic stability tasks like wt shifts,
reaching, trunk rotation
g) Training using dynamic surface like a ball/ foam
h) Stepping/ marching in place/ heel raises/ toe
offs
i) Movement transitions
j) Altering visual inputs like eyes closed/ reduced
lighting
k) Partial wall squats

24. GAIT TRAINING
• Practice walk with vertical poles
• Verbal cues to ‘walk tall’
• Use of overhead harness
• Visual/ auditory cues
• Use of grids/ footprints to improve foot placement
• Marching in high stepping pattern to improve step
height
• Sidestepping/crossed step walking
• Altering the support surface
• Community walking
• Stair climbing, ramp walking
• Weight supported treadmill training

25. CARDIOPULMONARY TRAINING
a) Diaphragmatic breathing exs.
b) Air- shift techniques
c) Thoracic mobility exs.
d) Exs. Of neck, shoulder &Trunk ms.
e) LE/UE ergometry
f) Aerobic pool program
g) Ex frequency 3-5 days/week

26. Equipment
Rolling Walkers are best – canes
& standard walkers are
frequently carried by the patient.
Shower chairs
Grab Bars
Raised Toilet Seats with
armrests.
Chairs with arms to assist
patient to lower themselves to
the chair without falling.

27. THANK YOU