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PARKINSONISM  NiharikaAgrawal ShwetaKolhatkar AnsuChacko Chi-Hsin Yu
What is parkinson’s disease? ,[object Object]
It has an insidious onset,[object Object]
Basal Ganglia
Functions of BG Motor planning and programming, internally generated movement Input from cortex=> thought=> motor plan=> select and inhibit specific strategies=> regulate movement (tone, force) Caudate nucleus: cognitive- awareness of body orientation in space (righting reflexes), behavior modification as per task requirement, motivation
Pathways
Pathophysiology  Parkinsons’ disease is idiopathic parkinsonism. •Substantia niagra pars compacta- degeneration of dopaminergic neurons •Dopaminergic neurons- cell bodies in SNpc=> axons in striatum •Dopamine deficiency- underactive direct pathway=> bradykinesia overactive  indirect pathway=> rigidity and tremors •Slow and progressive disease •Neuron degeneration progresses- Cytoplasmic inclusion (Lewy) bodies; loss of striatal dopamine receptors=> decrease in dopamine binding sites=> loss of effectiveness of medication (L-dopa)
	Signs & Symptoms Rigidity •Cog-wheel vs lead pipe •‘heaviness and stiffness of limbs’ •Resistance to all passive movement •Progression: proximal=> distal=> whole body Unilateral=> bilateral Stretch reflexes are normal#
Resting tremors- Involuntary oscillation at 4-6 Hz •Pill-rolling tremors of the hand •Aggravating factors: emotional stress, fatigue. •Relieving factors: Relaxation •Absent: voluntary activity, sleep. •Fluctuations in frequency and intensity  •Postural tremor: head & trunk, upright posture 
Akinesia  Bradykinesia Hypokinesia: Reduced amplitude  Disturbances in attention and depression=> compound these signs. Influenced by degree of rigidity, fluctuations in drug action and stage of disease.
Postural deviations: Weakness: trunk extensor muscles > flexor muscles=> stooped posture, increased flexion of neck, trunk,  hips and knees=> changes the center-of-alignment, positioning patient at forward limits of stability
Gait Deviations Generalized loss of extension at hip, knee and ankle and decrease in trunk and pelvic motion                                                Decreased arm swing and stride length Small and shuffling steps, loss of normal heal toe progression  Abnormal stooped posture                   Festinating gait (Progressive increase in speed with the shortening in stride) Takes multiple short steps to catch his own COM
Complications Freezing spells Reduced aerobic capacity Falls Osteoporosis Fractures sleep disorders Contractures & deformities Adverse effects of medication Constipation Facial muscle rigidity leading to Masked face
Postural instability •Abnormal and inflexible posture responses •Increased body sway. Narrow BOS or divided attention increase instability and may compromise balance. •Dynamic balance and perturbations may elicit an abnormal pattern of co-activation- due to: •Difficulty in feed-forward anticipatory adjustments of postural muscles during voluntary movements- due to RIGIDITY, REDUCED MUSCLE TORQUE PRODUCTION, WEAKNESS and LOSS OF AVAILABLE ROM IN TRUNK AND OTHER MUSCLES. •Visuospatial impairment and problem with sensorimotor adaptation. Unable to perceive the upright positon due to visual, proprioceptive and vestibular perception abnormalities.
Visual defects: blurred vision, photophobia, conjugate gaze, saccadic eye movements. •Speech, voice and swallowing: Mutism, Dysphagia, Sialorrhea etc. Respiratory dysfunction Depression and social isolation
MEDICAL MANAGEMENT SYMPTOMATIC THERAPY: Levodopa Carbidopa – Sinemet: decarboxylase inhibitor  Adverse effects- orthostatic hypotension, arrhythmias, constipation,  delusions, hallucinations Dopamine Agonist : bromocriptine, ropinirole ‘wearing- ‘off’ state or end-of-dose deterioration’ Later, on-off phenomena- appearance and disappearance of signs and symptoms
ANTICHOLINERGICS: Ethopropazine, benztropine, trihexyphenidyl + l-dopa => reduce motor fluctuations Adverse effects: dizziness, blurred vision, dryness of mouth, constipation, urinary retention ANTI-DEPRESSANTS:  TCA,  benzodiazepines NEUROPROTECTIVE THERAPY:  Slows progression  Monoamine oxidase inhibitors (MAO):  improves intracerebral metabolism of dopamine
Surgical techniques Pallidotomy Stereotaxic thalamotomy Deep brain stimulation of STn/GPi- superior to medication Cortical stimulation Gene therapy
CASE STUDY: Mr. K  Age: 72 y/o male  Diagnosis: Parkinson’s Disease (PD) 5 years ago. Hoehn & Yahr stage 3  On a combination of medication.  Activity: Able to perform most ADLs alone, fatigues easily has been having  Activity limitation: Difficulty in rolling, completing sit<>stand, and walking in small spaces.  He recently fell when carrying groceries in from the car.  Mr. K was referred to physical therapy and has not previously received PT.
		ICF model of Mr. K Parkinson’s Disease Stage III Impairements Rigidity, Akinesia, Impaired motor planning & balance, Postural instability, Impaired muscle performance, gait deviations, aerobic decon Activity Limitations Difficulty in bed mobility & sit to stand  Participation Restriction Community ambulation  Environment factors Personal factors Age, comordities, Hoehn& Yahr Stage 3 , No PT taken Combination of Medication, Progressive dis
Test and Measures Balance testing- TUG, ABC scale, berg balance, functional reach test, dynamic gait index.  Co-ordination testing- RAMS, finger to nose, heel to shin test. Task analysis- ADLs, IADLs, Functional Independence Measure Disease specific outcome measures:  ,[object Object]
Unified Parkinson’s Disease Rating Scale (UPDRS)SF 36. 6MWT Gait observational analysis. Environment assessment. 
Prognosis  Difficult  Severity of disease symptoms  Different patient response  No standardization in onset  Mr.K ‘s prognosis ----  Guarded Rationale :  ,[object Object]
No co- morbidities
 High risk of falls
 Progressive disease,
Stage 3. ,[object Object]
Goals:  Mr. K will roll from supine to side-lying within 5 seconds by performing an effective segmental rolling independently by end of 2 weeks.  Mr. K will stand from a standard chair/ bed within 8 secs independently with hand support on a firm supporting surface without loosing balance by end of 2 weeks.  Mr. K will stand on a firm surface without loosing balance with eyes open 
Goals
Plan of Care Patient , family and caregiver education : Patient and his/her caregivers must be educated about, The clinical presentation and progressive nature of the disease  Importance of mobility and maintaining activity level and modifications ( explain)  Techniques and strategies to manage and maintain the condition  Prevention of complications & impairements Importance of exercises  Lifestyle modification Energy conservation  Active participation in social activities  Encouragement and motivation Daily diary
Coordination, communication &Documentation Co-ordinate with caregivers and family about the medications
Intervention  Relaxation techniques: => reduce rigidity and increase flexibilitySlow, rhythmic, segmental rotations PNF techniques:  ,[object Object]
Contract relax techniques.Diaphragmatic breathing  Meditation  Conscious relaxation and release of muscle tension(called chaitanyasan- an asana of yoga) 7, 9 Relaxation audio tape Gentle yoga and tai chi 7,8
Sit to Stand Rocking forward- backward=> relaxation=> enhance ability to shift weight forwards Visual and verbal Cues With gait belt on. 7- 10 reps, RPE Progression
STRETCHING + STRENGTH Stretching  PNF, trunk range of motion  Progression Spinal flexibility exercises
•Strengthening exercises- stress on extensor muscles Warm water strengthening exercise Bridging, sit to stand, step up and down-17 to 35 cm- 10 reps, downhill walking Intensity: 60% of 1 RM,  Volume: 10-12 reps, 2-3 sets, 2 minute rests between sets Exercise session: 20 minutes Frequency: alternate days •Swiss ball ****, roll exercises, one leg stance •Gym music •Pelvic floor exercises Respiratory muscle training
BALANCE TRAINING •Narrow Base Of Support- eyes open=> closed Tandem- eyes open=> closed single leg standing eyes open=> closed pertubations standing on foam •Rocker board •Heel and toe raises •Ball toss on rocker board, trampoline and foam •Marching on trampoline Swiss ball exercises
Computerized Dynamic Posturography

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Parkinsons disease

  • 1. PARKINSONISM NiharikaAgrawal ShwetaKolhatkar AnsuChacko Chi-Hsin Yu
  • 2.
  • 3.
  • 5. Functions of BG Motor planning and programming, internally generated movement Input from cortex=> thought=> motor plan=> select and inhibit specific strategies=> regulate movement (tone, force) Caudate nucleus: cognitive- awareness of body orientation in space (righting reflexes), behavior modification as per task requirement, motivation
  • 7. Pathophysiology Parkinsons’ disease is idiopathic parkinsonism. •Substantia niagra pars compacta- degeneration of dopaminergic neurons •Dopaminergic neurons- cell bodies in SNpc=> axons in striatum •Dopamine deficiency- underactive direct pathway=> bradykinesia overactive  indirect pathway=> rigidity and tremors •Slow and progressive disease •Neuron degeneration progresses- Cytoplasmic inclusion (Lewy) bodies; loss of striatal dopamine receptors=> decrease in dopamine binding sites=> loss of effectiveness of medication (L-dopa)
  • 8. Signs & Symptoms Rigidity •Cog-wheel vs lead pipe •‘heaviness and stiffness of limbs’ •Resistance to all passive movement •Progression: proximal=> distal=> whole body Unilateral=> bilateral Stretch reflexes are normal#
  • 9. Resting tremors- Involuntary oscillation at 4-6 Hz •Pill-rolling tremors of the hand •Aggravating factors: emotional stress, fatigue. •Relieving factors: Relaxation •Absent: voluntary activity, sleep. •Fluctuations in frequency and intensity  •Postural tremor: head & trunk, upright posture 
  • 10. Akinesia  Bradykinesia Hypokinesia: Reduced amplitude Disturbances in attention and depression=> compound these signs. Influenced by degree of rigidity, fluctuations in drug action and stage of disease.
  • 11. Postural deviations: Weakness: trunk extensor muscles > flexor muscles=> stooped posture, increased flexion of neck, trunk, hips and knees=> changes the center-of-alignment, positioning patient at forward limits of stability
  • 12. Gait Deviations Generalized loss of extension at hip, knee and ankle and decrease in trunk and pelvic motion                                                Decreased arm swing and stride length Small and shuffling steps, loss of normal heal toe progression  Abnormal stooped posture                   Festinating gait (Progressive increase in speed with the shortening in stride) Takes multiple short steps to catch his own COM
  • 13. Complications Freezing spells Reduced aerobic capacity Falls Osteoporosis Fractures sleep disorders Contractures & deformities Adverse effects of medication Constipation Facial muscle rigidity leading to Masked face
  • 14. Postural instability •Abnormal and inflexible posture responses •Increased body sway. Narrow BOS or divided attention increase instability and may compromise balance. •Dynamic balance and perturbations may elicit an abnormal pattern of co-activation- due to: •Difficulty in feed-forward anticipatory adjustments of postural muscles during voluntary movements- due to RIGIDITY, REDUCED MUSCLE TORQUE PRODUCTION, WEAKNESS and LOSS OF AVAILABLE ROM IN TRUNK AND OTHER MUSCLES. •Visuospatial impairment and problem with sensorimotor adaptation. Unable to perceive the upright positon due to visual, proprioceptive and vestibular perception abnormalities.
  • 15. Visual defects: blurred vision, photophobia, conjugate gaze, saccadic eye movements. •Speech, voice and swallowing: Mutism, Dysphagia, Sialorrhea etc. Respiratory dysfunction Depression and social isolation
  • 16. MEDICAL MANAGEMENT SYMPTOMATIC THERAPY: Levodopa Carbidopa – Sinemet: decarboxylase inhibitor  Adverse effects- orthostatic hypotension, arrhythmias, constipation,  delusions, hallucinations Dopamine Agonist : bromocriptine, ropinirole ‘wearing- ‘off’ state or end-of-dose deterioration’ Later, on-off phenomena- appearance and disappearance of signs and symptoms
  • 17. ANTICHOLINERGICS: Ethopropazine, benztropine, trihexyphenidyl + l-dopa => reduce motor fluctuations Adverse effects: dizziness, blurred vision, dryness of mouth, constipation, urinary retention ANTI-DEPRESSANTS: TCA, benzodiazepines NEUROPROTECTIVE THERAPY:  Slows progression  Monoamine oxidase inhibitors (MAO):  improves intracerebral metabolism of dopamine
  • 18. Surgical techniques Pallidotomy Stereotaxic thalamotomy Deep brain stimulation of STn/GPi- superior to medication Cortical stimulation Gene therapy
  • 19.
  • 20. CASE STUDY: Mr. K  Age: 72 y/o male  Diagnosis: Parkinson’s Disease (PD) 5 years ago. Hoehn & Yahr stage 3  On a combination of medication.  Activity: Able to perform most ADLs alone, fatigues easily has been having  Activity limitation: Difficulty in rolling, completing sit<>stand, and walking in small spaces.  He recently fell when carrying groceries in from the car.  Mr. K was referred to physical therapy and has not previously received PT.
  • 21. ICF model of Mr. K Parkinson’s Disease Stage III Impairements Rigidity, Akinesia, Impaired motor planning & balance, Postural instability, Impaired muscle performance, gait deviations, aerobic decon Activity Limitations Difficulty in bed mobility & sit to stand Participation Restriction Community ambulation Environment factors Personal factors Age, comordities, Hoehn& Yahr Stage 3 , No PT taken Combination of Medication, Progressive dis
  • 22.
  • 23. Unified Parkinson’s Disease Rating Scale (UPDRS)SF 36. 6MWT Gait observational analysis. Environment assessment. 
  • 24.
  • 26. High risk of falls
  • 28.
  • 29. Goals: Mr. K will roll from supine to side-lying within 5 seconds by performing an effective segmental rolling independently by end of 2 weeks.  Mr. K will stand from a standard chair/ bed within 8 secs independently with hand support on a firm supporting surface without loosing balance by end of 2 weeks.  Mr. K will stand on a firm surface without loosing balance with eyes open 
  • 30. Goals
  • 31. Plan of Care Patient , family and caregiver education : Patient and his/her caregivers must be educated about, The clinical presentation and progressive nature of the disease  Importance of mobility and maintaining activity level and modifications ( explain)  Techniques and strategies to manage and maintain the condition  Prevention of complications & impairements Importance of exercises  Lifestyle modification Energy conservation  Active participation in social activities  Encouragement and motivation Daily diary
  • 32. Coordination, communication &Documentation Co-ordinate with caregivers and family about the medications
  • 33.
  • 34. Contract relax techniques.Diaphragmatic breathing  Meditation Conscious relaxation and release of muscle tension(called chaitanyasan- an asana of yoga) 7, 9 Relaxation audio tape Gentle yoga and tai chi 7,8
  • 35. Sit to Stand Rocking forward- backward=> relaxation=> enhance ability to shift weight forwards Visual and verbal Cues With gait belt on. 7- 10 reps, RPE Progression
  • 36. STRETCHING + STRENGTH Stretching  PNF, trunk range of motion  Progression Spinal flexibility exercises
  • 37. •Strengthening exercises- stress on extensor muscles Warm water strengthening exercise Bridging, sit to stand, step up and down-17 to 35 cm- 10 reps, downhill walking Intensity: 60% of 1 RM,  Volume: 10-12 reps, 2-3 sets, 2 minute rests between sets Exercise session: 20 minutes Frequency: alternate days •Swiss ball ****, roll exercises, one leg stance •Gym music •Pelvic floor exercises Respiratory muscle training
  • 38. BALANCE TRAINING •Narrow Base Of Support- eyes open=> closed Tandem- eyes open=> closed single leg standing eyes open=> closed pertubations standing on foam •Rocker board •Heel and toe raises •Ball toss on rocker board, trampoline and foam •Marching on trampoline Swiss ball exercises
  • 40.
  • 41. Gait training •↑stride length, ↑BOS, improve heel-toe gait pattern, ↑contralateral trunk m’t & arm swing •Stepping forward and backward •Stopping, starting, changing direction, turning •Sidestepping and crossed- step walkingPNF activity of braiding •Visual + auditory cues •Treadmill -body weight support-downhill Medication
  • 42. Aerobic ex. •Submaximal ex.: 50~70% HR peakevery alternate day •6MWT •Walking •Upper/lower extremity ergometryfor postural instability and high risk of fall-stationary or seated ergometry
  • 43.
  • 44. Mobility exercises - pursing lips, miling, frowing,wincing ,chewing, biting etc, movements of the tongue, swallowing,.Use of mirror in all these activities  Home exercise-Teach self relaxation rocking chair at home 6
  • 45. Other Evidences Based interventions, Tai Chi Yoga Kayaking Tango style dancing Karate Water aerobics
  • 46. References 1)O sullivan 2)Management of individuals with PD: rationale and case studies 3)Voss DE, Ionta MK, Myers BJ: Proprioceptive Neuromuscular Facilitation: Patterns and Techniques, ed 3- Philadelphia, PA, Harper & Row,Publishers Inc, 1985 FIND IT 4)Bobath B: Adult Hemiplegia: Evaluation and Treatment, ed 2. London, England, William Heinemann Medical Books Ltd, 1978 5)Stockmeyer S: An interpretation of the approach of Rood to the treatment of neuromuscular dysfunction. Am J Phys Med 46:900- 954, 1967 6)143 in sullivan FIND IT 7)Relaxation an yoga 8)Tai chi 9)Cochrane Database Syst Rev. 2006 Jan 25;(1):CD004998. Meditation therapy for anxiety disorders. Krisanaprakornkit T, Krisanaprakornkit W, Piyavhatkul N, Laopaiboon M.

Hinweis der Redaktion

  1. Mutism: reduced vital capacity=&gt; reduced air expended during phonation=&gt; whispering or mutismReduced range of movement and mobility and uncontrolled rate of movement of muscles of phonation, resonation, respiration. dysphagia, sialorrhea, hypokinetic dysarthria, monotone/monopitch speech, imprecise or distorted articulation, uncontrolled speech rate
  2. Cortical stimulation Experiments to assess chronic cortical stimulation of the motor area of monkeys with 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine-induced parkinsonism have shown an improvement in PD symptoms.Gene therapyOn the basis of the assumption that the hyperactive STN would deliver increased glutamate excitotoxin to the nigral dopaminergic cells, an adeno-associated virus vector containing an isoform of glutamic acid ecarboxylase has been used to transform the glutamatergic STN of rats into a GABAergic structure
  3. •Hoehn and Yahr Stage 3: Impaired righting reflexes; unsteadiness when turning or rising from chair; some activities are restricted but patient can live independently and continue some forms of employment
  4. Attributable to presence of RIGIDITY, reduced segmental dissociation impaired postural stability and balance,akinesia ( deficit in preparatory phase of movement control or ‘start hesitation’ deficit in response programming ) Assess the patient by timing the task of rolling he performs.Also analyse the movement and its qualityKeep the time as a quantifiable goal, progress accordingly.Intervention :
  5. Tai chi -