PARKINSON’S DISEASE AND OTHER 3) AKINETIC/ CLASS III/ MULTISYSTEM ATROPHY

- Aka rigid syndromes with parkinsonism/

MOVEMENT DISORDERS parkinsonian plus syndromes
- Neurodegenerative diseases that affect the
substantia nigra & produce parkinsonian
GENERAL MEDICAL BACKGROUND symptoms along with other neurological signs
- Includes: striatonigral degeneration (SND), Shy-
Drager syndrome, progressive supranuclear
I. DEFINITION palsy (PSP), olivoponto cerebellar atrophy
(OPCA), cortical basal ganglionic degeneration
- During the early stages, (+)rigidity &
PARKINSON‘S DISEASE
bradykinesia then with cognitive impairment
 aka Primary Parkinsonism/ Paralysis agitans/ True 4) SHY- DRAGER SYNDROME
PD - Manifested by seborrhea, sialorrhea,
 A chronic, progressive disease of the nervous hyperhydrosis, penile dysfunction & OH
system characterized by the cardinal features of:
 Tremors 5) PROGRESSIVE SUPRANUCLEAR PALSY
 Rigidity, - Loss of upward gaze & then later part of the
 Akinesia/ Bradykinesia disease, loss of lateral gaze
 Postural instability
 Described as ―shaking palsy‖ by James Parkinson in 6) HYPERKINETIC DISORDERS
1817 a. Chorea
- associated with Huntington‘s disease
Has two subgroups: - characterized by rapid, involuntary,
a. Postural Instability Gait Disturbance (PIGD) irregular & jerky movements
- The dominant symptoms include postural
instability & gait disturbances TYPES:
b. Tremor predominant - Huntington‘s disease- an AD disorder of
- With tremors as the dominant feature chromosome 4p
- Tardive dyskinesia- secondary to prolonged
Other terms: use of neuroleptic drugs
 PARKINSONISM- refers to a group of disorders that - Sydenham‘s- common among children & is
produce abnormalities of the basal ganglia related with rheumatic fever d/t
streptococcal infection
 BASAL GANGLIA
 once damaged, can either result in a b. Athethosis
hyperkinetic or hypokinetic motor disturbance. - Slow, writhing, sinusoidal movements d/t
There are 2 pathways of the signals: affectations of the globus pallidus
 Direct pathway which facilitates the flow of
signals to the thalamus thus allowing c. Ballismus
movement - Flinging, hurling & ballistic movements of
 Indirect pathway which inhibits information the extremities
flow & thus suppresses other movements - Primarily axial & proximal
 The neurotransmitters involved in the flowing of - d/t involvement of the subthalamic nucleus
signals include the: GABA, Dopamine,
Glutamate, Acetylcholine d. Dystonia
- Twisting, bizarre movements & if prolonged
contraction occurs, this results in dystonic
II. CLASSIFICATION posturing

1) PRIMARY PARKINSONISM/ CLASS I e. Tremors

- Idiopathic - Rhythmic, involuntary movements resulting
from alternate contraction & relaxation of
2) SECONDARY PARKINSONISM/ CLASS II/ opposing muscles
ACQUIRED PARKINSONISM
a. Post infectious Parkinsonism f. Tics
- Viral infection - Characterized as repetitive, intermittent &
- Influenza epidemics of encephalitis stereotypical movements
lethargic - Usually involves males
b. Toxic Parkinsonism - Gilles de la Torrette (smacking, puckering
- Industrial poisons & chemicals which or barking, there‘s also coprolalia &
includes Mn, Carbon disulfide, CO, cyanide palilalia)
& methanol
- Common among miners III. EPIDEMIOLOGY
c. Pharmacological  Age: >55yo
- Drugs that interfere with dopaminergic  Mean age of onset: 58-62yo
mechanisms either presynaptically or  Onset: insidious with slow rate of progression
postsynaptically such as neuroleptics  Males > Females
(Haloperidol/Haldol)
- Also antidepressants (Amitriptyline) & IV. ETIOLOGY–based on classification
antihypertensives (Methyldopa of high  Parkinsonism- abnormalities of BG
dosage)  Parkinson‘s Disease- MC form; idiopathic
d. Metabolic  Secondary Parkinsonism- different identifiable
- Disorders of Ca metabolism that causes causes (virus, toxins, drugs, tumors)
BG calcification  Parkinson-plus Syndrome- conditions that
- Disorders such as hypothyroidism, mimic PD but caused by other neuroregulatory
hyperparathyroidism, hypoparathyroidism & disorders
Wilson‘s disease

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V. PATHOPHYSIOLOGY  There‘s also (+)myerson‘s sign which is
characterized by a sustained blink response
 Degeneration of dopaminergic neurons that produce with repetitive tapping over the glabella
dopamine 5. Gait disturbances
 These neurons have their cell bodies in the  Decreased velocity
substantia nigra pars compacta & their axons are  Hip, knee, ankle motions are decreased
sent to the striatum  Decreased stride length & reciprocal arm swing
 At least 80% of neurons degenerate before  (+) small shuffling steps with (-) heel to toe
symptoms emerge. progression
 Loss of dopaminergic neuron results in reduction of  (+) festinating gait characterized by progression
spontaneous movement in speed & shortening of stride
 There can also be a decrease of the binding sites for  There can also be anteropropulsive gait or
dopamine in the BG retropulsive gait
 Develops a characteristic cytoplasmic inclusion 6. Swallowing & Communication Dysfunction
bodies called Lewy bodies as disease progresses  Dysphagia
 There is deficiency also of other neurotransmitters  Sialorrha
 Serotonin  Hypokinetic dysarthria & with advanced cases,
 Norepinephrine there is mutism
 Loss of dopamine results in an overactive indirect 7. Visual & Sensorimotor disturbances
pathway that is thought to underlie akinesia & rigidity  Blurred vision
 An underactive direct pathway is thought to be  Impaired conjugate eye movements & saccadic
responsible for bradykinesia eye movements
 Decrease blinking
AREAS OF PREDILECTION  Numbness & paresthesias
 Dorsal motor nucleus of the vagus, hypothalamus,  Postural stress syndrome can cause pain
locus caeruleus, cerebral cortex & autonomic  Akathisia which is extreme motor restlessness
ganglia that interferes with relaxation
8. Cognitive & behavioral changes
 Dementia
VI. CLINICAL MANIFESTATIONS  Loss of executive functions
 Bradyphrenia
 Rigidity  Perceptual deficits especially with spatial
 one of the clinical hallmarks organization
 refers to resistance to passive motion  Depression
 typically unequal in distribution  Dysthmic disorder which is atypical depression
 Patient c/o heaviness & stiffness of the limbs with intermittent episodes of severe anxiety
 Initially proximal muscles  Hallucinations & delusions
 Insomnia
Types: 9. Autonomic dysfunction
 Cogwheel  Excessive perspiration, greasy skin,
 Leadpipe thermoregulatory abnormalities & bladder
dysfunction
 Akinesia & Bradykinesia  Decreased GIT motility
10. Cardiopulmonary
 moments of freezing can occur,deficit in the
 OH
preparation phase of movement
 Cardiac arrhythmias
 the latter is the most diabling symptom
 Decreased forced expiratory volume, forced
vital capacity, with higher residual volume
 Micrographia
 Edema
 Tremor
 initial symptom VIII. DIAGNOSIS
 Slow frequency of about 4-7 cycles/ second No single definitive test
 ―pill rolling‖ of the hand but can also involve  Based on history & clinical exam
the feet, lips, tongue & jaw  At least two of the four cardinal features are
 (+) postural tremor which disappears during present
sleep  CT scan and MRI

 Postural instability
 (+) ability to maintain a steady position but IX. DIFFERENTIAL DIAGNOSIS
unable with dynamic activities
Parkinson‘s Disease must be differentiated from
other conditions, especially those presenting
VII. COMPLICATIONS with tremor. Parkinsonism refers to any
condition that causes a combination of the
1. Poverty of Movement movement abnormalities seen in PD—such as
 As tasks become more complex, difficulty tremors, slow movement, impaired speech, or
increases muscle stiffness—resulting from the loss of
 Can also be caused by fatigue & loss of dopamine-containing neurons. Not everyone
motivation who has parkinsonism has PD.
2. Fatigue
 Performance decreases with great physical Other diagnoses that you should consider:
effort  Essential tremor-produces tremors, or uncontrolled
3. Masked face shaking, in the hands and sometimes the head, that
 There‘s infrequent blinking & lack of expression progress over time. The tremor is not associated
 (+) blepharoclonus with eyelids closed with other PD symptoms. Progressive supranuclear
 (+) blepharospasm which is involuntary palsy (PSP)- loss of vertical eye movements.
4. Musculoskeletal changes
 Loss of flexibility  Progressive supranuclear palsy (PSP)- is a brain
 Contractures are common disorder that affects walking and balance, often
 Deformities also include kyphosis, some also resulting in falls. The condition can also cause
with scoliosis
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 problems with vision & eye movement.PSP does not NUTRITIONAL MANAGEMENT
usually respond to medication.  no to high CHON diet
 Multiple system atrophy (MSA)- is a rare,
progressive nervous system disorder that may share SURGICAL MANAGEMENT
some of the same symptoms as PD. Other  Stereotaxic surgery
symptoms of MSA may include poor coordination, - surgical lesioning of the brain
slurred speech, problems with breathing &  Pallidotomy
swallowing, & constipation. - producing a destructive lesion in the BG that
tends to reduce globus pallidus internus
 Corticobasal degeneration (CBD)- alien limb, excessive activity
spasticity, cortical sensory loss.  Thalamotomy
 Deep brain stimulation
 Diffuse Lewy Body Dementia (LBD)- early - implantation of electrodes in the brain that block
dementia presenting within 2 years of motor the signals that cause symptoms
symptoms  Transplantation
- of cells capable of delivering dopamine into the
Early clinical features that suggest an atypical striatum of the patients with advanced PD
Parkinsonism rather than PD include the following:
 Falls at presentation or early in the disease
 Poor response to Levodopa
 Symmetry at disease onset PHYSICAL THERAPY EXAMINATION,
 Rapid disease progression EVALUATION & DIAGNOSIS
 No tremor
 Dysautonomia (eg. Urinary incontinence, fecal
incontinence, cathetherization for urinary retention, I. POINTS OF EMPHASIS ON EXAMINATION
persistent erectile failure, prominent symptomatic
orthostatic hypotension) 1) Cognition
 MMSE
2) Affective & psychosocial
X. PROGNOSIS  Geriatric Depression Scale/ Beck
Depression Inventory
 An estimate of the stage and severity of the disease 3) Sensory integrity
can be made by using the Hoehn-Yhar Classification 4) Pain
of Disability Scale. It provides a useful measure for  McGill Pain Questionnaire & VAS
charting the progression of the disease. Stage 1 is 5) Visual function
used to indicate minimal disease involvement, 6) ROM, MMT
whereas stage 5 is indicative of severe deterioration 7) Posture, Gait
in which the patient is confined to bed or a 8) Motor function
wheelchair.  Rigidity, bradykinesia with slowed reaction
time & prolonged movement time, tremors,
 Patients who have a young age at onset or who are postural instability
tremor predominant typically demonstrate a more 9) Dysphagia & Speech impairments
benign progression and a relatively good prognosis. 10) Autonomic changes
11) Cardiorespiratory
 Rapid progression= poor prognosis 12) Skin integrity & condition
13) Functional status
 FIM
 Katz Index of Independence in ADLs
14) General & disease specific health measures
GENERAL HEALTHCARE MANAGEMENT
 Unified PD Rating Scale, Sickness Impact
Scale, PD Questionnaire-39
I. MEDICAL, SURGICAL, AND
PHARMACOLOGICAL MGT HOEHN & YAHR CLASSIFICATION OF DISABILITY SCALE
STAGE I Minimal/absent; unilateral involvement if (+)
- No direct cue
STAGE II Minimal bilaterally/ but independent in ADL &(-
PHARMACOLOGICAL MANAGEMENT
)postural instability
 Monoamine oxidase B
- reduce oxidative stress on neurons or inhibit
STAGE III Bilateral; independent in ADL with postural
toxins on neurons
instability
 Dopamine replacement
- aka L-dopa,Levodopa, Carbidopa
STAGE IV Bilateral involvement; needs assistance with
- mainstay treatment
ADLs; independent with ambulation
- a precursor of dopamine, raises the dopamine
levels in the basal ganglia
STAGE V Confined to bed or wheelchair
- L-dopa & Carbidopa are combined to allow
greater amount of the L-dopa to enter BBB
- initial improvement seen among PD pts is
known as ―honeymoon period‖ II. PROBLEM LIST
- ―wearing off‖ or end of dose deterioration is  Rigidity
characterized by worsening of symptoms during  Contractures
the expected time frame of medication  Postural instability
effectiveness  Impaired balance
- there are dyskinesias presented as facial  Impaired coordination
grimace, lip twitching or tongue protrusion  Impaired Gait and gait disturbances
 Decreased daily functional activities
- ―drug holidays‖
 Anticholinergics  Fatigue
- tremors
III. PT DIAGNOSIS
 Antiviral
 Decreased functional activities 2° to impaired
- has antiparkinson effects
muscle performance
 Dopamine agonists
 Impaired muscle performance 2° to damage of
- may improve function of dopamine receptors
the BG
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 Respiratory Exercises
 DBE
PHYSICAL THERAPY PROGNOSIS, POC & Aerobic Conditioning
INTERVENTION  Submaximal intensities (50-70% of heart rate
reserve)
 Frequency: 3-5 days/week
I. PLAN OF CARE
 to decrease rigidity Group and Home Exercises
 to prevent contractures  Low impact aerobics
 to promote body awareness for postural
instability Patient and Family Education
 to improve balance and coordination  Clinical presentation of the disease
 to increase participation in daily functional  Strategies to manage symptoms
activities  Preventive measures to minimize the secondary
 to conserve energy complications and impairments
 Strategies for energy conservation and ensuring
II. INTERVENTION
activity participation
Motor learning strategies
 In the early stage, practice can be expected to
improve learning and performance.
 Large number of repetitions to develop
procedural skills
 Long and complex movement sequence should
be broken down into component parts
 In favor of a blocked practice order, thereby
reducing the effects of contextual interference
 Task should be modified and minimized
 With advanced cases, compensatory strategies
are utilized

Relaxation Exercises
 Gentle rocking to produce generalized
relaxation of excessive muscle tension d/t
rigidity
 PNF technique of Rhythmic Initiation helps
overcome the effects of rigidity
 Diaphragmatic breathing during exercises
 Stress management techniques are an
important adjunct to relaxation training
 Jacobson progressive relaxation techniques

Flexibility
 AROM and PROM exercises are used to
improve flexibility. AROM exercises emphasize
active motions and PROM exercises work
within the pt‘s available ROM to maintain range.
 Stretching techniques to elongate muscles. Can
also be combined with joint mobilization
techniques to reduce tightness of the joint
capsule or of ligaments around a joint. Stretch
should maintain at least 20-30 secs/3-5x/20-
30mins
 Passive positioning can also be used to stretch
tight muscles and soft tissues.
 Address contractures.

Mobility
 As well as controlled mobility
 Include the muscles of the face

Balance
 “Kitchen sink exercises” consists of heel-rises
and toe-offs, partial wall squats and chair rises,
single limb stance with side-kicks or back-kicks,
and marching in place.

Gait training
 Designed to lengthen stride, broaden BOS,
improve stepping, improve heel-toe gait pattern,
increase contralateral trunk movement and arm
swing, inc speed & provide a program of regular
walking.
 For improving upright alignment: have the pt
walk with vertical poles (pole walking) and
verbal cues to ‗walk tall‘
 PNF patterns can be used
 Provide visual cues as well as auditory cues

Functional Adaptations
 Of assistive devices
 Appropriate shoes

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