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Parkinson’s Disease

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

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Parkinson’s Disease

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  1. Parkinson’s Disease Chapter 18 Physical Rehabilitation Prepared by: Pethuel M. Pomaloy

  2. 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

  3. 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

  4. 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

  5. Etiology • 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

  6. Etiology 2. Secondary Parkinsonsim • A. Postencephalitic Parkinsonism • influenza epidemics of encephalitis lethargica(1917 to 1926) • onset of parkinsonian symptoms typically occurred after many years

  7. Etiology 2. Secondary Parkinsonsim • B. Toxic Parkinsonism • Environmental toxins (pesticides) • Industrial chemicals (carbon disulfide, carbon monoxide, cyanide, methanol) • Most common: Manganese

  8. 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

  9. Etiology 3. Parkinson-Plus syndrome • Neurodegenerative diseases that affects substantianigra and produce parkinsonian symptoms along with other neurological signs • Striatonigral degeneration (SND) • Shy-Drager syndrome • Progressive supranuclear palsy • Olivopontocerebellar atrophy • Cortical basal ganglionic degeneration

  10. 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)

  11. Pathophysiology • Degeneration of the dopaminergic neurons in the BG in the pars compactus of the substantianigra • As neurons degenerate, presence of cytoplasmic inclusion bodies calledLewy Bodies • Onset of motor symptoms 30-60% degeneration

  12. Pathophysiology

  13. 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, globuspallidusinterna and substantianigra pars reticulata to midbrain tegmentum • Inhibits/ decreases thalamocortical projections

  14. 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

  15. 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)

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  21. 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

  22. 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

  23. Clinical Presentation Nonmotor Symptoms • Speech Disorders • Hypokinetic dysarthria • Decreased voice volume, monotone, imprecise articulation, uncontrolled speech rate • Mutism

  24. 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

  25. 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

  26. 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

  27. 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

  28. Clinical Presentation • Sleep disorder • excessive daytime sleepiness • insomnia • dream enacting behaviors such as agitation, physical activity during sleep

  29. 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

  30. Clinical Course • Progressive, long sublicinical period • Patients at young age/ tremor predominant: more benign progression • cardiovascular disease and pneumonia: MC of death

  31. 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

  32. 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

  33. Medical Management • Management is directed at slowing disease progression • Increasingly more challenging over time as disease progresses

  34. 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)

  35. Pharmacological Management 1. 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

  36. Pharmacological Management • 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

  37. 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

  38. 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

  39. 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 benztropinemesylate (Congentin) • adverse effects: blurred vision, dry mouth, dizziness and urinary retention

  40. 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

  41. 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

  42. Nutritional Management • High protein diet can block effectiveness of L-Dopa • High calorie – low protein diet (no more than 15% of calories)

  43. 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

  44. 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

  45. 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

  46. 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)

  47. 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

  48. 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

  49. 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

  50. Physical Therapy Intervention • Motor Learning Strategies • blocked practice rather than random practice • structured instructional sets • external cues • Visual • Rhytmic Auditory Stimulation (metronome) • Multisensory cueing

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