PARKINSON’S DISEASE • Average age of onset: 50-60 yrs old

o Early onset: <40 y.o

(Shaking Palsy, Paralysis Agitans)
o Young onset: 21-40 y.o
o Juvenile onset: <21 yo
DEFINITION:
ETIOLOGY:
• Is a progressive disorder of the
central nervous system (CNS) with Parkinsonism
both motor and nonmotor symptoms
• A group of disorder with primary
• Degeneration of dopaminergic
disturbances in the dopamine system
neurons in the BG in the pars
of Basal Ganglia
compactus of the substantia nigra
o Primary PD
that produce dopamine
▪ Idiopathic
▪ MC type of PD
Cardinal Features: o Secondary PD
▪ with known etiology
• Rigidity
▪ LC type of PD
• Bradykinesia
o Parkinson’s Plus
• Resting Tremor ▪ mimic PD
• Postural Instability
Primary PD

ANATOMY: • Idiopathic PD
• Genetic
Basal Ganglia
o Gene: PINK1, PARK1, LRRK2
• Slowly progressive disorder of CNS
with motor and non-motor
symptoms
• Progressive loss of dopaminergic
cells that produces DA in the
Substantia Nigra
Secondary PD

• Post-infectious
o Encephalitis Lethargica
• Post Traumatic PD
EPIDEMIOLOGY:
o 2° repetitive Microtrauma to
• A common disease that affects 1 brain
million Americans; 7-10 million o Common in boxers
people worldwide o Dementia Pugilistica aka
• M>F commonly Punch-Drunk Syndrome
 • Toxic PD 7. Dopaminergic Neuron Degeneration:
o MC – Manganese Selective Vulnerability
o Pesticides
8. Neurotransmitter Imbalance: Dopamine
o Cyanide
Deficiency
o Carbon Disulfide
o Ethanol 9. Parkinsonian Symptoms
o 1 Methyl-4 Phenyl-1236-
Tetrahydropyridine (MPTP) Explanation:
• Metabolic PD
o Wilson’s Disease aka • Risk Factor: Genetic Predisposition
Hepatolenticular o Individuals with a family
Degeneration history of Parkinson's disease
▪ Buildup of Copper in are at an increased risk.
the Brain Genetic mutations, such as
those in the LRRK2 and SNCA
• Drug Induced PD
genes, have been identified
o Neuroleptic Drugs
as potential contributors.
o Anti-depressant Drugs
o Anti-HTN Drugs • Altered Protein Function: Alpha-
synuclein Aggregation
Parkinson’s Plus o Genetic mutations or
environmental factors can
• A group of neurodegenerative
lead to the misfolding and
diseases can affect the substantia
aggregation of alpha-
nigra and produce parkinsonian
synuclein protein within
symptoms along with other
neurons. This abnormal
neurological sign
accumulation forms Lewy
bodies, a characteristic
PATHOPHYSIOLOGY: pathological feature of
Parkinson's disease.
1. Risk Factor: Genetic Predisposition
• Neuronal Dysfunction:
2. Altered Protein Function: Alpha-synuclein Mitochondrial Impairment
Aggregation o Alpha-synuclein aggregates
disrupt normal mitochondrial
3. Neuronal Dysfunction: Mitochondrial
function. Mitochondrial
Impairment
impairment causes a decline
4. Oxidative Stress: Reactive Oxygen Species in energy production and an
(ROS) increase in oxidative stress
within dopamine-producing
5. Inflammation: Microglial Activation
neurons.
6. Impaired Autophagy: Clearance • Oxidative Stress: Reactive Oxygen
Dysfunction Species (ROS)
 o Mitochondrial dysfunction
results in an elevated
production of reactive
oxygen species (ROS). ROS
cause damage to cellular
components, including lipids,
proteins, and DNA, leading to
increased neuronal stress.
• Inflammation: Microglial Activation
o The presence of aggregated
alpha-synuclein and
oxidative stress triggers an
inflammatory response.
Microglial cells, the brain's
resident immune cells,
become activated, releasing
pro-inflammatory cytokines
and exacerbating neuronal
damage.
• Impaired Autophagy: Clearance
Dysfunction
o The accumulation of
misfolded proteins
overwhelms the cellular
clearance mechanisms,
particularly autophagy.
Autophagy dysfunction
further contributes to the
persistence of alpha-
synuclein aggregates and
impairs the removal of
damaged cellular
components.
• Dopaminergic Neuron
Degeneration: Selective
Vulnerability
o Dopamine-producing
neurons in the substantia
nigra are selectively
vulnerable to the toxic
effects of alpha-synuclein
aggregation, oxidative stress,
and inflammation. This leads
to progressive degeneration
and loss of these neurons
over time.
• Neurotransmitter Imbalance:
Dopamine Deficiency
o As dopaminergic neurons
degenerate, there is a
significant reduction in
dopamine production and
release in the striatum, a
critical area for motor
control. The decline in
dopamine levels results in
motor symptoms
characteristic of Parkinson's
disease, such as tremors,
bradykinesia, and rigidity.
• Parkinsonian Symptoms
o The culmination of these
pathological processes
manifests as the classical
motor symptoms of
Parkinson's disease.
Additionally, non-motor
symptoms, such as cognitive
impairment and autonomic
dysfunction, may also arise
due to widespread
neurodegeneration.
Stages of Parkinson’s disease:
• Stage 1
o Lesions are found in the
medulla oblongata (dorsal
IX/X nucleus or intermediate
reticular zone)
• Stage 2 • Lead pipe rigidity is a sustained
o Involve lesions of the caudal resistance to passive movement,
raphe nuclei, gigantocellular with no fluctuations
reticular nucleus, and • Rigidity is often asymmetrical
coeruleus subcoeruleus
complex ❖ Bradykinesia
• Stage 3 • Refers to slowness of movement
o Involvement of the and is one of the cardinal
nigrostriatal system is features of PD
apparent (pars compacta of • Weakness, tremor, and rigidity
the substantia nigra) may contribute to bradykinesia
• Stage 4 but do not fully explain it.
o Lesions are also found in the • Bradyphrenia – slowness of
cortex (temporal mesocortex thought can contribute to
and allocortex) bradykinesia
• Stage 5 • Akinesia – refers to a poverty of
o Pathology is extended to spontaneous movement
involve the sensory • Hypomimia – masked facial
association areas of the expression, with significant social
neocortex and pre-frontal consequences
neocortex • Hypokinesia – refers to slowed
• Stage 6 and reduced movements
o Pathology is extended to • Micrographia – handwriting that
involve the sensory may start out strong but becomes
association areas of the smaller and smaller as writing
neocortex and premotor proceeds
areas
❖ Tremor
CLINICAL MANIFESTATIONS: • Involuntary shaking or oscillating
movement of a part or parts of
Primary Motor Symptoms the body resulting from
❖ Rigidity contractions of opposing
• One of the clinical hallmarks of PD muscles.
and is defined as increased resistance • Resting tremor
to passive motion o Present at rest,
• Cogwheel rigidity is a jerky, suppressed briefly by
ratchet like resistance to passive voluntary movement, and
movement as muscles alternately disappears with sleep.
tense and relax. Occurs when a o Hand – Mc pill-rolling
tremor coexists with rigidity ▪ 3-5 Hz
 ❖ Postural Instability
• Abnormalities of posture and
balance, resulting in postural
instability.
Secondary Motor Symptoms
❖ Muscle Performance
o Fatigue is among the most
common symptoms reported
❖ Motor Function
❖ Gait
o Festinating gait – progressive
increase in speed with a
shortening of stride.
▪ Anteropulsive
(forward festinating
gait)
▪ Retropulsive
(backward festinating
gait)
Non-motor Symptoms
❖ Sensory Symptoms
o 50% experience paresthesias
and pain including sensations
of numbness, tingling, cold,
aching pain, and burning.
❖ Dysphagia
o Impaired swallowing
o Present in as many as 95% of
patients and is the result of
rigidity, reduced mobility,
and restricted range of
movement
o Four phases of swallowing:
▪ Oral preparatory
▪ Oral
▪ Pharyngeal
▪ Esophageal
• Sialorrhea – excessive drooling as
a result of increased saliva
production and decreased
spontaneous swallowing.
❖ Speech Disorders
o Speech is impaired in
75% to 89% of
patients
o Hypokinetic
dysarthria –
characterized by
decreased voice
volume, monotone
sound, imprecise or
distorted articulation,
and uncontrolled
speech rate.
❖ Cognitive Dysfunction
o Can be mild or severe
o PD dementia occurs in
approximately 20% to
40% of the patients
o Bradyphrenia –
slowed thinking
❖ Depression and Anxiety
o Major depression is
reported in 40% of
patients
o Dysthymic disorder –
characterized by
chronic depression
and dysphoric mood,
resulting in poor
appetite or
overeating, insomnia
or hypersomnia, low
energy, low self-
esteem, and poor
concentration.
 o Anxiety is a common signs and elements of
symptom in PD, functional status.
occurring in 38% of o Stage I is used to indicate
patients. minimal disease involvement,
❖ Autonomic Dysfunction whereas stage V is indicative
o Seborrhea – increased oil of severe deterioration in
secretion of the sebaceous which the patient is confined
glands of the skin to bed or a wheelchair
o Seborrheic dermatitis – oily,
chafing, and reddened skin
o Gastrointestinal disorders
o Constipation
o Urinary incontinence
o Erectile dysfunction
o Orthostatic hypotension
(OH) – sharp drop in BP that
occurs with position changes
❖ Sleep Disorders
o Excessive daytime
somnolence (sleepiness)
o Insomnia (disturbed sleep
pattern)

OUTCOME MEASURES:
❖ Unified Parkinson’s disease Rating
Scale (UPDRS)
o Gold standard for measuring
the progression of PD since DIFFERENTIAL DIAGNOSIS:
1987 PD SIMILARITIES LEWY
o Renamed to Movement BODY
Disorder Society-sponsored DEMENTI
revision of the Unified A
Parkinson’s Disease Rating Motor Both are Cognitive
Scale (MDS-UPDRS) symptoms characterized symptoms
❖ Hoehn-Yahr Classification of are more with protein are more
Disability prominent aggregates pronounce
o It provides a broad measure and may containing d, motor
for charting the progression precede alpha synuclein symptoms
cognitive may just
of the disease using motor
symptoms coexist
 Positive Both Individuals Surgical Mx:
response conditions can may have
to manifest with a negative • Ablative Surgery
dopaminer parkinsonian reaction to o The surgical lesioning of the
gic features dopaminer brain
medicatio gic o The lesion reduces excessive
ns medicatio globus pallidus internus (GPi)
ns inhibitory activity that results
Fluctuatio Both are Fluctuatio in tonic thalamic hypoactivity
ns in progressive ns in • Deep Brain Stimulation (DBS)
alertness neurodegenera attention o Involves the implantation of
are not a tive disorders and electrodes onto the brain
typical alertness
where they block nerve
feature are
signals that cause symptoms
common
o A pacemaker is implanted in
the chest, with a thin wire
MEDICAL/SURGICAL: that goes under the skin to
the brain electrodes
Pharmacological Mx:
o Its major advantage is its
• Anticholinergics potential to alter tremor
o Dry mouth, dizziness, without producing an
blurred vision irreversible brain lesion
Tachycardia, dry mouth, • Neural Transplantation
nausea, vomiting, o Studies involve the grafting of
confusion embryonic stem cells from
• Dopamine Replacement umbilical cord blood or fetal
o Dry mouth, dizziness, cells.
blurred vision o Adverse side effects such as
Tachycardia, dry mouth, serious dyskinesias in more
nausea, vomiting, than 50% of patients have
confusion been reported
• Dopamine Agonists o Patients usually undergo
o Nervousness, dyskinesias, immunosuppression
insomnia, hallucinations, following surgery to reduce
nausea, confusion the risks of graft rejection
• Amantadine
o Lightheadedness
PT ASSESSMENT: o PNF technique of rhythmic
initiation (RI) – movement
• Pt Hx
progresses from passive to
• OI
active-assistive to lightly
• FIM resisted or active movement
• ROM was specifically designed to
• MMT help overcome the effects of
• Posture rigidity PD.
• Gait o Bilateral symmetrical PNF D2
• DTR flexion patterns – used to
expand the restricted chest
PT INTERVENTION: and promote shoulder ROM.
• Flexibility Exercises
• Motor Learning Strategies o ROM exercises emphasize
o Structured instructional sets active motions that are
– improve movement speed performed two to three times
and consistency (e.g. walking a day
patterns with focused o Exercises should focus on
instructions of “swing your strengthening the weak,
arms”, walk fast” or “take elongated extensor muscle,
large steps”) while lengthening the
o Visual cues – include shortened, tight flexor
stationary floor markings and muscles
dynamic transportable cues o D2 flexion patterns in the UE
o Rhythmic auditory o D1 extension pattern in the LE
stimulation (RAS) – use of a o Traditional stretching
metronome beat or a steady techniques
beat from a musical listening o Passive positioning is used to
device stretch tight muscles and soft
o Pulsed cues – to the earlobe tissues
or the hand o Bedridden patients benefit
o Multisensory cueing – use of from weights applied to
both visual and auditory reduce hip and knee flexion
cueing contracture
• Relaxation Exercises • Strength Training
o Hooklying, lower trunk o Indicated for patients with
rotation, or sidelying rolling, primary muscle weakness
or upper and lower trunk and insufficient central
segmental rotations can be activation of the motor unit
used to promote relaxation as well as for disuse weakness
 associated with prolonged
inactivity.
o Patient should consistently
exercise at the same time
after a medication dose on
alternate days.
o Exercise machines may be
safer than free weights as
movements are more
controlled, especially for
patients who demonstrate
dyskinesia at peak dose or
cognitive changes.
• Functional Training
o Moving in bed - emphasis on
segmental rotation patterns
since it is beneficial for
patients with very stiff trunks
to reach over and initiate
movement
o Sitting posture - anterior and
posterior tilts, side-to-side
tilt, pelvic clock exercises can
be practiced while sitting on a
therapy ball
▪ Sitting activities with
weight shifting
▪ PNF extremity pattern
o Sit-to-stand transitions
▪ Initial rocking forward and
backward
▪ Cueing strategies to assist
forward rocking movements
▪ Practice from a firm raised
seat to promote ease of rise 
▪ Modified wall slides for
preparatory lead-up activity
to sit-to-stand activity
o Standing training activities
▪ The patient needs to first gain
the fully upright position with
symmetrical weight bearing
over the base of support
(BOS).
▪ Tactile cueing or light
resistance to hip extensors on
the anterior pelvis
▪ Weight shifts and rotational
movements upon standing
▪ Lateral side steps or step ups
▪ Standing with UEs extended
and hands weightbearing on
a wall
▪ Mobilizing facial muscles
▪ Practice lip pursing,
movements of the tongue,
swallowing and facial
movements.
o Adaptive and Supportive Devices
▪ Satin sheets and pajamas
have sometimes been helpful
to enhance bed mobility
▪ Select firm chairs with
armrests and avoid soft, low
seats such as a low sofa
▪ Raised toilet seat and toilet
rails
▪ Flat heel or toe wedge may
slow down propulsive gait,
whereas a raised heel or heel
wedge may diminish a
retropulsive gait pattern
▪ Walkers with wheels are
particularly hazardous, and
are likely to increase a
festinating gait.
▪ The height of the assistive
device should not promote
increased flexion of the trunk
o Balance Training
▪ Weight shifts
▪ Reaching
▪ Axial rotation of the head and
trunk combined with
reaching
▪ Externally induced
perturbation
o Cardiopulmonary Training
▪ Air shifts
▪ Upper body resistance training
exercises
▪ Raising and lowering a dowel
with light weights
▪ Pool exercises
▪ LE ergometry
o Schenkman’s Approach
▪ Relaxation
▪ Breathing exercises
▪ Passive muscle stretching
and positioning
▪ AROM and postural
alignment
▪ Weight shifting
▪ Balance responses
▪ Gait activities
▪ Patient home exercises
o Flewitt-Hanford Exercises
▪ These exercises were
developed to help improve
gait of Parkinson patients
▪ A result of adaptation to gain
control of forward
progression and balance