PARKINSON’S DISEASE

DEFINITION
 A chronic, progressive disease of the nervous
system due to degeneration of dopamine-
producing cells in the substantia nigra
characterized by rigidity, bradykinesia,
resting tremor, and postural instability
Other names:
 Paralysis agitans
 True PD
 Idiopathic Parkinson’s disease
 Shaking palsy
 Anatomy
Extrapyramidal system – eliminates unwanted
movements for smooth voluntary motor
activity
1. Basal ganglia
2. Subthalamic nucleus
3. Substantia nigra
4. Reticular formation
5. Red nucleus
Cell bodies in the basal ganglia
1. Putamen
2. Globus pallidus – regulates muscle tone
3. Caudate nucleus - coordination

Striatum/Neostriatum (controls large

subconscious movements) = caudate
nucleus + putamen
Paleostriatum/Pallidum = globus pallidus
Lenticular nucleus = globus pallidus + putamen
Corpus striatum = lenticular nucleus + caudate
nucleus
Dopamine – main inhibitory neurotransmitter
from the basal ganglia
Acetylcholine – main excitatory
neurotransmitter within the corpus striatum

Circuit involved in PD:

Striatum  Substantia Nigra  Thalamus 
Cerebral Cortex
EPIDEMIOLOGY
 58-62 y/o – mean age of onset
 M > F
 Kyphosis – most common postural deformity
 Pneumonia – one of the leading causes of

death
ETIOLOGY
Parkinsonism – a group of disorders that
produce abnormalities of the basal ganglia
function
1. Primary parkinsonism – most common cause
2. Secondary parkinsonism – results from a
number of different causes
3. Parkinson-plus syndromes – conditions with
symptoms of multiple system degeneration
Primary parkinsonism
Parkinson’s disease – Idiopathic parkinson’s disease
 True PD, paralysis agitans, shaking palsy
 Groups:
 Postural instability gait disturbed
 Tremor predominant
Secondary parkinsonism
1. Post-infectious parkinsonism – caused by viral
infection
 Encephalitis lethargica – “sleeping sickness”
 Presence of headache and drowsiness progressing to
coma
 Cryptococcal meningitis – inflammation of meninges
caused by Cryptococcus

2. Toxic parkinsonism – from industrial poisons and

chemicals
 Manganese – most common
 Synthetic heroin – causes severe parkinsonism
3. Pharmacological parkinsonism – drugs that
interfere with dopaminergic mechanisms
 Neuroleptic drugs
 Antidepressant drugs
 Antihypertensive drugs
* * withdrawal of these agents usually
reverses the symptoms

4. Metabolic parkinsonism – caused by disorders of

calcium metabolism that result in basal ganglia
calcification
 Hypothyroidism – decrease secretion of thyroxine,
triiodothyronine, and calcitonin which are essential for
normal metabolism and growth
Parkinson-plus syndromes
1. Akinetic/rigid syndromes with parkinsonian
features
 A group of neurodegenerative disease that can affect the
substantia nigra and produce parkinsonian symptoms
 Striatonigral degeneration, Shy-drager syndrome (early
autonomic failure), huntington’s disease (hereditary
disease caused by a defect in a single gene with symptoms
of unsteady gait and jerky involuntary movements
[chorea])
PATHOPHYSIOLOGY
 
Degeneration of dopaminergic neurons
↓
Decrease dopamine production
↓
80% degeneration: signs become evident
↓
Loss of melanin-containing neurons
↓
Changes in depigmentation
↓
Progression: development of Lewy’s bodies
↓
Loss of dopaminergic neurons
↙ ↘
Loss of inhibitory influences decrease binding sites for dopamine
↓ ↓
Tremor, rigidity loss of effectiveness of L-dopa
CLINICAL MANIFESTATIONS
Cardinal features:
 Rigidity

 Bradykinesia

 Resting tremor

 Postural instability

Triad of PD:
 Rigidity

 Bradykinesia

 Resting tremor
Rigidity
 resistance to passive motion; not velocity dependent
 Felt uniformly in muscles on both sides of the joint
 Usually affects asymmetrically
 Affects proximal muscles first, especially the shoulder and

neck. Progresses to the face and extremities  loss of arm

swing during gait and loss of bed mobility
 Caused by damage to the globus pallidus, ↓ dopamine, ↑

acetylcholine

Types:
1. Cogwheel – jerky, ratchetlike resistance to passive
movement as the muscles alternately tense and relax
2. Leadpipe – constant, uniform resistance without fluctuations
Webster’s rating scale for rigidity:
0 – no involvement
1 – Detectable rigidity in the neck and
shoulder. One or both arms show mild,
negative, resting rigidity
2 – Moderate rigidity in the neck and shoulder.
Presence of resting rigidity
3 – Severe rigidity in the neck and shoulder.
Resting rigidity cannot be relieved by
medications
Bradykinesia
 slowness of movement
 Akinesia – severe form
 When it affects the facial muscles  masked facies
(hypomimia)
 ↓ speed, range, amplitude
 Inability to change direction while walking, difficulty
walking around objects, difficulty standing
 Influenced by rigidity and depression
 Involvement of muscles innervated by cranial nerves III,
VII, IX
 Due to failure of the basal ganglia to integrate sensory
information so that motor planning and facilitation of
movement are altered
Grading for bradykinesia:
0 – absent
1 – minimum slowness
2 – moderate slowness, poverty of movement
3 – marked slowness, poverty of movement, hesitancy, arrest of
ongoing movement
4 – severe slowness, poverty of movement, unable to move all 4 limbs
simultaneously
 
 
Webster’s rating scale for bradykinesia of the hands:
0 – no involvement
1 – detectable slowing of pronation-supination rate evidenced by
difficulty in handling tools, buttoning clothes and writing
2 – moderate slowing of pronation-supination rate evidenced by
moderate impairment of hand functions. Writing is greatly impaired
including micrographia
3 – severe slowing of pronation-supination rate. Patient is unable to
write or button clothes
Resting tremor
 involuntary oscillation of a body part at rest
 Most common complaint and initial symptom
 Begins as “pill-rolling” tremor of the index
finger and thumb
 Usually disappears during voluntary movement
 Postural tremor (head and trunk) – can be seen
when muscles are used to maintain an upright
position against gravity. In the LE, tremor is
felt during supine position
 Due to decreased levels of serotonin
Grading for tremor:
0 – no detectable tremor
1 – less than 1 inch of peak-to-peak
movement at rest in the limb
2 – maximum tremor envelope of not more
than 4 inches. Tremor is severe but constant
and the pt retains some control of the hand
3 – tremor enveloped over 4 inches. Tremor is
constant and severe. Pt cannot get free from
tremor while awake. Writing and feeding are
impossible
Postural instability
 most disabling, least specific
 due to degeneration of globus pallidus
 balance is lost due to loss of reactive processes needed to

adjust posture and regain equilibrium

 extensor muscles of trunk – demonstrate greater

weakness, resulting to a flexed, stooped posture with

increased flexion of the neck, trunk, hips, and knees
 pt falls backward or to the side
 tandem stance – narrowing of BOS
 abnormal pattern of coactivation, insufficient neural

activation of agonist muscles, delayed muscle recruitment

and that once initiated is characterized by
asynchronization
 kyphosis – most common postural deformity
Other clinical manifestations
1. Start hesitation – difficulty initiating when, where and how to move
2. Micrographia – abnormally small handwriting
3. Freezing episodes (motor blocks)
4. Hypomimia – reduction in expressiveness of the face
5. Myerson’s sign – a sustained blink response produced after repetitive tapping
over the bridge of the nose
6. Decreased motor learning
7. Festinating gait – increased speed, decreased stride. Pt take multiple short steps
to catch up with his COM to avoid falling
8. Paresthesia and pain – usually in the tight shoulders as a result from postural
stress syndrome secondary to lack of movement, rigidity, and faulty posture
9. Dysphagia
10. Sialorrhea – excessive drooling
11. Hypokinetic dysarthria – decreased voice volume, monotone speech, distorted
articulation and uncontrolled speech rate
12. Dementia
13. Depression
14. Impaired ANS
15. Orthostatic hypotension
16. Airway obstruction
17. Restrictive lung dysfunction
DIAGNOSIS
 At least 2 of the 4 cardinal features are
present
 Exclusion of Parkinson-plus syndromes is

necessary (presence of extrapyramidal signs

that are bilateral symmetrical and do not
respond to L-dopa and dopamine agonists)
Tools
1. MRI
2. Positron emission tomography
3. Single-photon emission computerized
tomography
PT Dx
1. Presence of tremor, festinating gait, flexed stooped
posture, expressionless face, rigidity, babinski reflex,
hyperreflexia, micrographia
2. Loss of hip and knee extension, ankle dorsiflexion,
shoulder flexion, elbow extension, dorsal spine and
neck extension, and axial rotation during ROM
3. Slow movement
4. Excessive drooling or sweating
5. Tonal changes in the shoulder and neck, trunk and
extremities
6. Rapid, monotonous, low volume with poor
articulation in speech
Pharmacology
Levodopa (L-dopa) – mainstay of symptomatic
treatment
◦ A metabolic precursor of dopamine that is able to cross
the BBB and raise the level of striatal dopamine in the BG
◦ Commonly administered with CARBIDOPA, which allows a
higher percentage of L-dopa to enter the CNS
◦ L-dopa is usually metabolized before reaching the brain
◦ SINEMET – most common carbidopa/L-dopa medication;
alleviates bradykinesia and rigidity, less effect on tremor

Selegiline – delays the primary endpoint at which pts

need to start taking L-dopa
◦ Monoamine oxidase inhibitor (drug class)
◦ Once L-dopa therapy is started, selegiline in combination
permits a lower dose to be used
Dopamine agonists – act directly on the
postsynaptic dopamine receptors
◦ Example: bromocriptine
◦ Reduces rigidity and bradykinesia

Anticholinergics – used in early, untreated PD

◦ Block cholinergic function and have the most
benefit moderating tremor and rigidity
◦ Examples: trihexyphenidyl, bentropin
Surgical management
Indications:
1. pts with advanced PD who respond poorly to
medications
2. pts who experience complications related to
pharmacotherapy
 Stereotactic surgery – surgical lesioning of the brain
◦ Pallidotomy – producing a destructive lesion in the
sensorimotor portion of the globus pallidus internus which
produces excessive GPi inhibitory activity that results in
tonic thalamic hypoactivity; indicated for rigidity and tremor
◦ Thalamotomy – producing a destructive lesion within the
ventral intermediate nucleus of the thalamus; reduces
longstanding tremor, improvement of rigidity
 Deep brain stimulation – implantation of electrodes
into the brain where they block nerve signals that
cause symptoms
 Neural transplantation – transplantation of cells

capable of surviving and delivering dopamine into

the striatum of pts with advanced PD; stem cells?????
PROGNOSIS
 Hoehn and Yahr Classification of Disability

Stage I - Minimal or absent; unilateral if

present
◦ Tremor of 1 limb
◦ Decreased arm swing
◦ Micrographia
◦ hypophonia
Stage II - Minimal bilateral or midline
involvement; balance not impaired
◦ Sx’s evident in Stage I, plus
◦ Bradykinesia
◦ Stoop posture
◦ Shuffling gait
Stage III - Impaired righting reflex;
unsteadiness when turning or rising from the
chair; some activities are restricted but pt is
independent
◦ Sx’s evident in Stages I & II, plus
◦ Pronounced gait disturbance
◦ Moderate general disability
Stage IV - All symptoms present and severe;
standing and walking possible only with
assistance
◦ Sx’s evident in Stages I, II & III, plus
◦ Significant disability
Stage V - Confined to bed or wheelchair
◦ Sx’x evident in Stages I, II, III & IV, plus
◦ Complete invalidism
 Positive prognostic features:
1. Early tremor

2. Rigidity

3. Family history

Negative prognostic features:

4. Bradykinesia

5. Akinesia

6. Postural instability

7. Gait difficulties

8. Cognitive defects

9. Late age of onset

PT Mx
Relaxation techniques
 A rocking chair is a good tool for pt

relaxation
 Rhythmic initiation
 Jacobson’s progressive relaxation techniques

– contract-relax
 Lower trunk rotation with the pt hook-lying

– to relax trunkal rigidity

ROM and mobility exercises
 ROM should focus on strengthening the weak

extensor muscles and stretch the tight flexor

muscles
 Prone-on-elbows and prone-on-extension –

improve thoracic extension

 PJM – to decrease tightness of joint capsule
 Bilateral symmetrical D2 flexion pattern –

activates extensors in order to straighten the

spine
 Standing balance with rhythmic stabilization
Breathing exercises – emphasis on diaphragmatic
breathing
Clinical restorator – for conditioning
Gait training
◦ Lengthen stride, widen the BOS
◦ Increase contralateral trunk movement and arm swing
◦ Place markers or blocks to help encourage the pt to
widen the stride and avoid shuffling the feet
PRE’s
US – over the tight structures especially the
shoulder
HMP
FES – emphasis on weak extensor muscles
HEP – walking exercise
OTHER MOVEMENT DISORDERS
Huntington’s disease
 Relentless, progressive, adult-onset, autosomal dominant disorder
that is associated with cell loss within a specific subset of neurons in
the caudate nucleus and putamen
 Cardinal features: involuntary movements, dementia, and behavioural
changes
 Clinical onset usually 30-50 years of age, fatal outcome usually
within 15-20 years
 Caused by mutant huntingtin
 Pneumonia and cardiovascular changes – most common primary
causes of mortality
 Depression – most common psychological dysfunction
 Hallmark: Chorea – excessive abrupt irregular spontaneous
involuntary movements
 Westphal variant: hypokinesia and rigidity
 Chorea does not respond to physical therapy
Hereditary ataxias
 can result from disorders of the cerebellum
or its connections
 Friedreich ataxia – most common syndrome.

It is a progressive disorder with the

presentation of limb and gait ataxia with
diminished muscle stretch reflexes, joint
position sense, and vibratory appreciation
Hereditary spastic paraparesis
 a group of inherited disorders in which the primary
symptoms are progressive bilateral lower extremity
spasticity and weakness caused by axonal degeneration in
the spinal cord, maximally in the corticospinal tracts and
the dorsal column fibers
 Other names: familial spastic paraplegia, Strumpell-Lorrain
syndrome
 Progressive difficulty walking – classic presenting symptom
 Cardinal features: symmetric lower extremity spastic
paresis, extensor plantar responses
 Tx: cold application, manual stretching techniques,
splinting, serial casting, posture and body mechanics
training, aerobic conditioning, and gait and dynamic
balance training
Dystonia
 movement disorder characterized by muscle
contraction resulting in twisting, turning, and
posturing as a result of sustained co-
contraction of the agonist and antagonist
 Tx: massage, slow stretching, US, gait

training and mobility

Tourette syndrome
 a constellation of symptoms including tic
disorders and comorbid neurobehavioral
problems
 Tics – involuntary, sudden, rapid, repetitive,

non-rythmic, stereotyped movements or

vocalizations
 Commonly involves the face, head and shoulders
(sniffing, blinking, frowning, shoulder shrugging, head
thrusting)
TAMA NA YAN,
INUMAN NA!