Parkinson’s Disease

PARKINSON’S DISEASEChapter 18 Physical RehabilitationPrepared 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

Etiology1. 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

Etiology2. Secondary Parkinsonsim

• A. Postencephalitic Parkinsonism• influenza epidemics of encephalitis lethargica (1917 to 1926)• onset of parkinsonian symptoms typically occurred after many

years

Etiology2. Secondary Parkinsonsim

• B. Toxic Parkinsonism• Environmental toxins (pesticides)• Industrial chemicals (carbon disulfide, carbon monoxide, cyanide,

methanol)• Most common: Manganese

Etiology2. 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

Etiology3. 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

Etiology3. 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 PresentationPrimary 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 PresentationPrimary 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 PresentationPrimary 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 PresentationPrimary 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 PresentationSecondary 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 PresentationSecondary 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 PresentationSecondary 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 PresentationNonmotor 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 PresentationNonmotor 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 PresentationNonmotor Symptoms• Speech Disorders

• Hypokinetic dysarthria• Decreased voice volume, monotone, imprecise articulation, uncontrolled speech

rate• Mutism

Clinical PresentationNonmotor 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

practiceI – minimal or absent, unilateral if presentII – minimal bilateral or midline involvement, balance not impairedIII – Impaired righting reflex, unsteadiness when turning or rising from chair

Some activities are restricted but patient can live independentlyIV – all symptoms present and severe, standing and walking only possible with assistanceV – 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 Management1. Levodopa/ Carbidopa (Sinemet)

• Primary benefits: controlling PD motor symptoms of bradykinesia 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 Management1. 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 Management1. 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 Management2. 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 Management3. 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 Management4. 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 ManagementImplications 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

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

THANK YOU FOR LISTENING