Transcript File

PARKINSON’S DISEASE
Chapter 18 Physical Rehabilitation
Prepared by: Pethuel M. Pomaloy
Characteristics
• Progressive disorder of CNS
• Disturbance in the dopamine system of basal nuclei
• Both motor and non-motor symptoms
• Cardinal Features:
• Rigidity
• Bradykinesia
• Tremor
• Postural instability
Incidence
• 1 million Americans
• 7 – 10 people worldwide
• Average age of onset: 50 – 60 years old
• 4 – 10%: Early onset PD (< 40 years old)
• Juvenile onset (< 21 y.o.)
• Young onset PD (21 – 40 y.o.)
• Men: 1.2 to 1.5 times more frequent
Etiology
• Parkinsonism
• Generic term used to describe a group of disorders with primary
disturbances in the dopamine system of the basal ganglia (BG).
• PD/ Idiopathic parkinsonism
• most common form (78%)
• Secondary parkinsonism
• results from a number of identifiable causes including viruses, toxins,
drugs, tumors etc.
• Parkinson-plus syndromes
• Conditions that mimic PD in some respects but are caused by other
neurodegenerative diseases
Etiology
1. Parkinson’s Disease
• first described as “shaking palsy” by James Parkinson in
1817
• Refers to cases where etiology is unknown or genetically
determined
• Clinical subgroups:
• Postural Instability and Gait Disturbed (PIGD)
• Tremor Predominant
Etiology
2. Secondary Parkinsonsim
• A. Postencephalitic Parkinsonism
• influenza epidemics of encephalitis lethargica (1917 to 1926)
• onset of parkinsonian symptoms typically occurred after many
years
Etiology
2. Secondary Parkinsonsim
• B. Toxic Parkinsonism
• Environmental toxins (pesticides)
• Industrial chemicals (carbon disulfide, carbon monoxide, cyanide,
methanol)
• Most common: Manganese
Etiology
2. Secondary Parkinsonsim
• C. Drug induced parkinsonsim (DIP)
• drugs that produce extrapyramidal dysfunctions that mimics sign
of PD
• interfere dopaminergic mechanisms
• Neuroleptic drugs: chlorpromazine, haloperidol, thirodiazine
• Antidepressant drugs: amitriptyline, amoxapine, trazodone
• Antihypertensive drugs: methyldopa (aldomet), reserpine
Etiology
3. Parkinson-Plus syndrome
• Neurodegenerative diseases that affects substantia nigra and
produce parkinsonian symptoms along with other neurological
signs
• Striatonigral degeneration (SND)
• Shy-Drager syndrome
• Progressive supranuclear palsy
• Olivopontocerebellar atrophy
• Cortical basal ganglionic degeneration
Etiology
3. Parkinson-Plus syndrome
• Multi-infarct vascular disease
• Alzheimer’s disease
• Diffuse Lewy body disease
• Normal pressure hydrocephalus
• Creutzfeldt-Jakob disease
• Wilson’s disease
• Juvenile huntington’s disease
• Diagnostic feature: do not show measurable improvement to anti-
parkinson medication such as levodopa (apomorphine test)
Pathophysiology
• Degeneration of the dopaminergic neurons in the BG in
the pars compactus of the substantia nigra
• As neurons degenerate, presence of cytoplasmic
inclusion bodies called Lewy Bodies
• Onset of motor symptoms 30-60% degeneration
Pathophysiology
Pathophysiology
• Direct Motor Loop
• Ventrolateral thalamus to Cortex (Supplementary Motor Area)
• Excitatory and facilitates discharge of cells in the SMA
• Indirect Motor Loop
• Involves the subthalamic nucleus, globus pallidus interna and
substantia nigra pars reticulata to midbrain tegmentum
• Inhibits/ decreases thalamocortical projections
Clinical Presentation
Primary Motor Symptoms
• Rigidity
• Increased resistance to passive motion that is constant regardless
of the task, amplitude or speed of movement
• Both agonist and antagonistic muscles
• Often assymmetrical during early stage
• Proximal muscles first
• Active movement, mental concentration, emotional stress increase
rigidity
• Types:
• Cogwheel: jerky, ratchet like, muscles alternate tense and relax
• Lead pipe: sustained resitance, (-) fluctuations
Clinical Presentation
Primary Motor Symptoms
• Bradykinesia
• Slowness of movement
• Insufficient recruitment of muscle force during initiation of
movement
• Akinesia – poverty of spontaneous movements; ex. Hypomimia
• Freezing episodes
• Hypokinesia – slowed and reduced movements (micrographia)
Clinical Presentation
Primary Motor Symptoms
• Tremor
• involuntary shaking or oscillating movement of a part or parts of the
body resulting from contractions of opposite muscles
• Resting tremor: suppressed by rest and disappears with sleep
• Postural tremor
• Action tremor – seen in advanced PD
Clinical Presentation
Primary Motor Symptoms
• Postural Instability
• Rare in first 5 years
• Abnormal and inflexible postural responses
• Difficulty in regulating feed forward and anticipatory judgements
• Weakness of antigravity muscles: adoption of a flexed, stooped
posture with increased flexion of trunk, neck, hips and knees
• LE: hip and knee flexors, hip rotators, adductors, PFors
• Spine: dorsal spine and neck flexors
• UE: shoulder adductors and IR, elbow flexors
• Frequent falls and fall injuries
Clinical Presentation
Secondary Motor Symptoms
• Muscle performance
• Reduction in strength that may be dopamine related
• EMG studies: motor unit recruitment delayed with
under-recruitment of muscles
• Disuse weakness
• Fatigue: difficulty in sustaining activity and experiences
weakness and lethargy as the day progresses
Clinical Presentation
Secondary Motor Symptoms
• Motor Function
• Motor planning deficits: loss of voluntary and automatic movement
responses
• Speed – Accuracy Trade-off
• Dual-task control problems
• Start Hesitation
• Motor learning deficits may be seen but not universal
Clinical Presentation
Secondary Motor Symptoms
• Gait
• 13-33% of patients presents with postural instability and gait
disturbance as their initial motor symptom
• Reduction in arm swing with assymetry
• Festinating gait
• progressive increase in speed with shortening of stride
• anteropulsive / retropulsive
• Problems in turning and changing direction
Clinical Presentation
Nonmotor Symptoms
• Sensory Symptoms
• Do not suffer primary sensory loss
• 50% experience paresthesias and pain, sensation of numbness, tingling,
cold, aching pain and burning
• Postural stress syndromes
• Proprioceptive and Visuospatial deficits
• Olfactory dysfunction: Anosmia
• Visual disturbance caused by conventional drugs (anticholinergics): blurred
vision, sensitivity to light (photophobia), eye pursuit may be jerky
• Decreased blinking
Clinical Presentation
Nonmotor Symptoms
•
Dysphagia
• present in 95% of patients with PD
• Result of rigidity, reduced mobility and restricted range
of movement
• Excessive drooling (sialorrhea): increased saliva
production, decreased spontaneous swallowing
• Can be present in all stages
Clinical Presentation
Nonmotor Symptoms
• Speech Disorders
• Hypokinetic dysarthria
• Decreased voice volume, monotone, imprecise articulation, uncontrolled speech
rate
• Mutism
Clinical Presentation
Nonmotor Symptoms
• Cognitive Dysfunctions
• mild (mildly impaired memory) or severe (psychosis)
• PD dementia occurs in approximately 20% to 40% of
the patients
• Bradyphrenia
Clinical Presentation
• Depression and anxiety
• Feelings of guilt, hopelessness, worthlessness, loss of energy, poor
concentration, deficits in short term memory, loss of ambition and
enthusiasm, suicidal thoughts
• Hypomimia
• Dysthmic d/o: chronic depression, poor appetite or overeating,
insomnia or hypersomnia, low energy, low self-esteem
• Panic attacks
• Social phobia
• Agoraphobia
• OCD, panic d/o
Clinical Presentation
• Autonomic dysfunction
• direct manifestation of disease
• thermoregulatory dysfunctions
• seborrhea and seborrheic dermatitis
• slow pupillary responses
• GI disorders: constipation, urinary incontinence
• erectile dysfunction
• diminished heart function
• orthostatic Hypotension
Clinical Presentation
• Autonomic dysfunction
• airway obstruction: (air trapping, lung inflation) most frequently
reported pulmonary problem
• restricted lung disease
• low FVC, low FEV1 and higher RV
• moderate edema d/t immobility
Clinical Presentation
• Sleep disorder
• excessive daytime sleepiness
• insomnia
• dream enacting behaviors such as agitation, physical activity
during sleep
Medical Diagnosis
• Made on the basis of history and clinical examination
• Diagnosis is made if at least two of the four cardinal
features are present
• Apomorphine testing
Clinical Course
• Progressive, long sublicinical period
• Patients at young age/ tremor predominant: more benign
progression
• cardiovascular disease and pneumonia: MC of death
Hoehn-Yahr Classification of Disability Scale
• Most widely used severity staging scale in clinical
practice
I – minimal or absent, unilateral if present
II – minimal bilateral or midline involvement, balance not impaired
III – Impaired righting reflex, unsteadiness when turning or rising from
chair
Some activities are restricted but patient can live independently
IV – all symptoms present and severe, standing and walking only
possible with assistance
V – confined to bed or wheelchair
Unified Parkinson’s Disease Rating Scale
• “Gold Standard” for measuring progression of PD
• Part I: Mentation, Behavior, Mood
• Part II: ADL
• Part III: Motor Examination
• Part IV: Complications of therapy
Medical Management
• Management is directed at slowing disease progression
• Increasingly more challenging over time as disease
progresses
Pharmacological Management
• Starting medication early has been shown to be
beneficial in slowing progression of disease
• 1. Levodopa/ Carbidopa (Sinemet)
• Levodopa: Gold standard drug therapy for PD
• Levodopa (L-dopa): precursor of dopamine, more than 99% of
levodopa is metabolized before reaching the brain
• Carbidopa: Decarboxylase inhibitor
• Available in Immediate release (IR) and Controlled release (CR)
Pharmacological Management
1. Levodopa/ Carbidopa (Sinemet)
• Primary benefits: controlling PD motor symptoms of bradykinesia
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and rigidity, initial burst of motor activity, increased strength
Honeymoon period: initial dramatic improvement in functional
status, presence of clear cut drug effectiveness
4-6 years therapeutic window, then wearing off state
Dyskinesias – involuntary movements that appear as facial
grimacing, twitching, puckering of lips and may progress to
choreathetoic movements of shoulders, arms and hands
Dystonia
On-off phenomenon
Pharmacological Management
1. Levodopa/ Carbidopa (Sinemet)
• Dyskinesias – involuntary movements that appear as facial
grimacing, twitching, puckering of lips and may progress to
choreathetoic movements of shoulders, arms and hands
• Dystonia
• On-off phenomenon
Pharmacological Management
1. Levodopa/ Carbidopa (Sinemet)
• unsupervised reduction or sudden discontinuation is
contraindicated
• dose related changes:
• Disabling psychiatric toxicity
• Depression
• GI changes
• CV changes
• Genitorurinary changes
• Sleep disturbance
Pharmacological Management
2. Dopamine Agonists
• designed to directly stimulate postsynaptic dopamine receptors
• pt.’s with declining response to levidopa and carbidopa may
benefit
• adverse effects similar with levodopa
• increased risk for impulse control disorders: (pathological
gambling, compulsive shopping, hypersexuality, overeating)
• Bromocriptine
Pharmacological Management
3. Anticholinergics
• Most benefit moderating tremor and dystonia
• have little or no effect on other PD symptoms
• Anticholinergic adverse effects include blurred vision, dry mouth,
dizziness and urinary retention
• trihexyphenidyl (Artane) and benztropine mesylate (Congentin)
• adverse effects: blurred vision, dry mouth, dizziness and urinary
retention
Pharmacological Management
4. Monoamine Oxidase B Inhibitors (MAO-B)
• MAO-B is the major enzyme that acts to degrade dopamine in the
brain
• Selegiline (deprenyl) and Rasagiline (Azilect)
• Permits lower dose of levodopa
• Adverse effects: mild nausea, dry mouth, dizziness, orthostatic
hypotension, confusion, hallucinations, and insomnia
Pharmacological Management
Implications for Physical Therapy
• Fully aware of the medications and potential adverse effects
• It is important to remember that patients on dopamine replacement
will develop motor complications at some point
• Timing of PT examination and intervention
Nutritional Management
• High protein diet can block effectiveness of L-Dopa
• High calorie – low protein diet (no more than 15% of
calories)
Deep Brain Stimulation
• implantation of electrodes in
brain blocking signals
• effective in treatment of
advanced PD
• Possible adverse effects:
Confusion, Headache, Speech
problem, gait disturbance
Physical Therapy Examination and
Evaluation
• 1. Cognitive Function
• Mini Mental State Examination
• 2. Psychosocial Function
• Geriatric Depression scale, Beck depression Inventory
• Hospital Anxiety and Depression Scale
• 3. Sensory Function
• 4. Musculoskeletal Function
• Joint Flexibility and posture
• Spinal ROM
• Muscle Performance
Physical Therapy Examination and
Evaluation
• 4. Musculoskeletal Function
• Muscle performance
• Strength and Endurance
• MMT, handheld and isokinetic dynamometry
• 5. Motor Function
• Rigidity
• Bradykinesia
• Movement time
• Reaction time
• Rapid alternating movements
• Dexterity
Physical Therapy Examination and
Evaluation
• 5. Motor Function
• Tremor
• Location, persistence, severity (amplitude)
• Postural control and balance (Berg balance Scale, Timed up and
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•
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Go test)
Gait
Fall Risk (Fall Risk diary)
Fatigue (Multidimensional Fatigue Inventory, Fatigue Severity
Scale)
Dyskinesia (Rush dyskinesia Scale)
Physical Therapy Examination and
Evaluation
• 5. Motor Function
• Tremor
• Location, persistence, severity (amplitude)
• Postural control and balance (Berg balance Scale, Timed up and
•
•
•
•
•
Go test)
Gait
Fall Risk (Fall Risk diary)
Fatigue (Multidimensional Fatigue Inventory, Fatigue Severity
Scale)
Dyskinesia (Rush dyskinesia Scale)
Swallowing and speech
Physical Therapy Examination and
Evaluation
• 6. Autonomic Function
• Cardiorespiratory Function
• 6 Minute/ 12 minute walk test
• Orthostatic Hypotension
• drop in systolic BP of 20 mmHg and 10 mmHg in diastolic BP and 10-
20% increase in pulse rate
• Integumentary Integrity
• Seborrhea and Seborrheic Dermatitis
• 7. Functional status
• Functional Independence Measure
Physical Therapy Examination and
Evaluation
• Disease Specific Measures
• Parkinson’s Disease Questionnaire (PDQ-39)
• Focuses on subjective report of the impact of PD on daily-life
• Parkinson’s Disease Summary Index
• 0-100
• provides useful indication of global impact of PD on health
status
Physical Therapy Intervention
• Motor Learning Strategies
• blocked practice rather than random practice
• structured instructional sets
• external cues
• Visual
• Rhytmic Auditory Stimulation (metronome)
• Multisensory cueing
Physical Therapy Intervention
• Exercise Training
• “Training big” program (High amplitude movements)
• Relaxation exercises
• Slow rocking
• Rhythmic Rotation
• Rhythmic Initiation (counters effects of rigidity)
• Bilat. Symmetrical PNF D2 flexion pattern with diaphragmatic breathing
• Flexibility Exercises
• Resistance Training
Physical Therapy Intervention
• Exercise Training
• Functional Training
• Bed Mobility Skills: Emphasize segmental rotation patterns than a log-
rolling pattern
• Sitting
• STS
• Standing
• Balance Training
• Should emphasize practice of dynamic stability tasks
• Locomotor Training
• Walk Tall, Walk fast, Take Large steps
• Braiding
Physical Therapy Intervention
• Spinal Orthotics
• Spinal bracing for postural deformities
• Pulmonary Rehabilitation
• breathing exercises
• exercise that recruit neck, shoulder and trunk muscles
• Manual techniques such as vibration and shaking
• Speech Therapy
• Aerobic Exercise
• Minimum: 3 sessions per week
• Daily walking with short multiple bouts (20-30) minutes throughout the
day for Pt.’s with lower functional capacity
Physical Therapy Intervention
• Group and Home Exercises
• Taichi classes
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