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Rehabilitation
of a person with
Parkinson’s Disease
Dr. Md. Mamunul Abedin
MBBS, BCS (Health), FCPS Trainee (PMR)
Dept. of Physical Medicine & Rehabilitation
National Institute of Neurosciences and Hospital, Dhaka
1
Parkinson’s Disease
Parkinson's disease (PD) is a neurodegenerative
disorder that affects predominately
dopaminergic neurons in a specific area of the
brain called substantia nigra.
2
Epidemiology
-The 2nd commonest neurodegenerative disease.
-Affects men and women of all races, all
occupations, and all countries.
-Mean age of onset is about 60 years. Frequency
increases with aging.
-The prevalence of the disease will be dramatically
increased in the next several decades.
3
Etiology
-Unknown (85 – 90%)
-Environmental Factors
Exposure to Pesticides
Rural Living
Drinking Well water
MPTP
Reduced risk with Cigarette smoking & Caffeine
-Genetic Factors
Gene mutations
Gene associations
4
Pathophysiology
The Pathological Hallmarks of PD:
-Depletion of the pigmented dopaminergic neurons in
the substantia nigra
-The presence of α-synuclein and other protein inclusions
in nigral cells (Lewy bodies)
-There are also other neuronal degenerations.
Loss of dopaminergic neurotransmission: Causes motor
symtomps
5
Pathophysiology (cont.)
Physiologically, Substantial Nigra is the major
output region of the Basal ganglia.
The output of Basal Ganglia provides inhibitory tone
to Thalamus & Brainstem, and in turn, control motor
functions,behavioral, emotional & cognitive functions.
Decreased neuronal activity in SN is associated with
movement facilitation via Dopaminergic projections.
6
Pathophysiology (cont.)
In PD,
Dopamine denervation/ Loss of Dopamine tone
Excessive inhibition of the Thalamus
Reduced activation of Cortical motor systems
Development of Parkinsonian features
7
Cardinal Features
Clinically, Parkinson’s Disease is characterized
by:
-Rest Tremor,
-Rigidity,
-Bradykinesia (Slowing), and
-Gait Impairment.
8
Clinical Features (Motor symptoms)
Positive Phenomena
▪ Tremor
 Resting Tremor
 Postural Tremor
 Re-emergent Tremor
-Suppressed by sleep and activity,
-Increased by fatigue or stress.
9
Clinical Features (Motor symptoms)
Positive Phenomena
▪ Rigidity
 Cogwheel type
 Lead pipe type
▪ Flexed Posture
Dominance of progravity flexor muscles
10
Clinical Features (Motor symptoms)
Negative Phenomena
▪ Bradykinesia
-Slowness of movement
▪ Loss of postural reflexes
▪ Postural instability
▪ Freezing phenomenon
-Transient inability to move.
11
Gait
▪ Slow to start walking
▪ Rapid, Short stride length, Tendency to
shorten (Festination)
▪ Reduction of arm swing
▪ Impaired balance on turning
Clinical Features (Motor symptoms)
12
Normal Findings
Power, Deep tendon reflexes, Plantar
Eye movements
Sensory & Cerebellar examination
Clinical Features
13
Clinical Features
(Other Motor features)
▪ Micrographia
▪ Masked facies (Hypomimia)
▪ Reduced eye Blinking
▪ Soft voice (Hypophonia)
▪ Dysphagia
14
Clinical Features (Non-motor Symptoms)
▪ Cognitive Impairment (Dementia)
▪ Neuropsychiatric Features:
Anxiety,
Depression,
Apathy,
Hallucinations/ Psychosis
▪ Sleep Disturbances & Hypersomnolence
▪ Fatigue, Drooling, Weight loss
▪ Sensory Disturbances (Pain)
15
Clinical Features (Non-motor Symptoms)
Autonomic Disturbances
▪ Orthostatic Hypotension
▪ Sphincter Disturbance
▪ Constipation
▪ Sexual Problems
Erectile failure,
Loss of Libido,
Hypersexuality
16
Differential Diagnosis
 Dementia with Lewy Bodies
 Multiple-System Atrophy (MSA)
 Progressive Supranuclear Palsy
 Secondary Parkinsonism
▪ Drugs
▪ Stroke
▪ Toxin
 Wilson’s Disease
 Huntington’s Disease 17
Investigation
Diagnosis is Clinical.
Structural imaging is normal.
Functional dopaminergic imaging is
abnormal in early stages (SPECT or PET)
To exclude Huntington’s/ Wilson’s
disease (in younger patients)
18
Management
Drug Therapy
▪ Levodopa
▪ Dopamine receptor agonists
▪ MAOI-B inhibitors
▪ COMT inhibitors
▪ Amantadine
▪ Anticholinergic drugs
19
Management (cont.)
Surgery
Deep Brain Stimulation
Rehabilitation
▪ Physiotherapy
▪ Occupational therapy
▪ Speech therapy
20
Rehabilitative Mx
Medical and Nursing
▪ Use of Firm bed
▪ Regular meals with proper diet (Low Protein)
▪ Measure vital capacity and enforce incentive
spirometry
▪ Gradual changing of positions, elastic stockings,
abdominal binder, sodium tablets, and possibly
pseudoephedrine, midodrine, and/or fludrocortisone
for orthostasis
21
Rehabilitative Mx
Medical and Nursing(cont.)
Bowel program for gastrointestinal hypomobility (stool
softeners, bulk-forming agents, cisapride, and
suppositories may be required)
Bladder evaluation and urodynamics; anticholinergics
(e.g., oxybutynin chloride [Ditropan]) for hyperreflexic
bladder
Artificial tears for lack of blinking
Sexual dysfunction evaluation
Anticholinergic medications before mealtime to help
facilitate oral and pharyngeal movements
22
Rehabilitative Mx
Gait Disturbances
▪ Shuffling gait pattern: Decreased step and stride length,
decreased cadence and velocity
▪ Festination
▪ Stooped (flexed) posture
▪ Freezing, “start hesitation”
▪ “Cautious” gait (fear of falling)
▪ Impaired balance and unsteadiness due to lightheadedness
▪ Dystonia, dyskinesia
23
Rehabilitative Mx
▪ Relaxation techniques
▪ Slow rhythmic rotational movements
▪ Gentle ROM and stretching exercises, quadriceps and hip extensor
isometric exercises
▪ Neck and trunk rotation exercises
▪ Back extension exercises and pelvic tilt
▪ Proper sitting and postural control (static and dynamic); emphasize
whole body movements
▪ Breathing exercises
▪ Functional mobility training, including bed mobility, transfer
training, and learning to rise out of a chair by rocking; may require a
chair lift
Rehabilitation for Gait Dysfunction
24
Rehabilitative Mx
▪ Functional mobility training:
Bed mobility,
Transfer training,
Learning to rise out of a chair by rocking; chair lift
▪ Stationary bicycle
▪ Training in rhythmic pattern to music or with auditory cues
▪ Standing or balancing in parallel bars (static and dynamic)
with weight shifting, ball throwing
Rehabilitation for Gait Dysfunction (cont.)
25
Rehabilitative Mx
▪ Slowly progressive ambulation training
Large steps using blocks to have patients lift legs,
Proper heel-to-toe gait patterns,
Feet 12–15 in. apart, arm swing;
Use inverted walking stick, colored squares, or stripes as
visual aids
▪ Use of assistive devices (may need a weighted walker)
▪ Aerobic conditioning (swimming, walking, cycling)
▪ Frequent rest periods
Rehabilitation for Gait Dysfunction (cont.)
26
Rehabilitative Mx
Movement Initiation
-Slow movement initiation.
-Result from delayed
activation of the motor cortex,
impeding one’s ability to
initiate and execute normal
movement.
-exacerbated with high-
complexity tasks.
-Difficulty in handwriting.
▪ It may be a strategy to
facilitate motor tasks.
▪
Rehabilitation
27
Rehabilitative Mx
Dyskinesia
-the excessive movement of
muscles in the trunk or
limbs that cannot be
controlled voluntarily.
-complication of levodopa
therapy after 7 or 8 years.
-due to highest conc of
Levodopa, and progressive
loss of dopamine neurons.
▪ If Mild, No measures
▪ If bothersome,
reduction of dose &
dosage of Levodopa
▪ Add Amantadine
Rehabilitation
28
Rehabilitative Mx
Dystonia
-the involuntary contraction of
a single muscle or multiple
muscles that cause an
abnormal posture,
-most common site is the foot
(contraction with flexion of the
toes and inversion of the entire
foot).
-Occurs when plasma
concentrations of Levodopa are
at their lowest and highest
▪ If at end of dose,
Ingestion of another dose.
▪ In Peak-dose dystonia,
if causes focal problem,
Local injection of
Botulinum toxin
Rehabilitation
29
Rehabilitative Mx
Orthostatic Hypotension
▪ Lifestyle modification and education
-Avoid warm or hot bath / A heavy meal /Excessive
straining while defecating and other tasks
-Taking high-fiber diets and stool softeners
▪ Gradual changing of positions (may use Tilt table)
▪ Compression leg stockings and abdominal binders.
▪ Omit unnecessary drugs
▪ Fludrocortisone or midodrine, if needed. 30
Rehabilitative Mx
Gastrointestinal
Problems
Swallowing Dysfunction
-Dysphagia due to loss of
lingual control
-Esophageal dysmotility
-Hypopharyngeal Stasis
-Aspiration
-Deficient positioning of
oesophagus
▪ Oral-motor exercise
by speech pathologist
▪ Chin-Tuck Maneuver
▪ Thickened liquids
Rehabilitation
31
Rehabilitative Mx
Gastrointestinal
Problems
Nutrition:
-At risk for weight loss
-Amino acids & Vit B6
hampers absorption of
Levodopa.
▪ Nutritional Consultation
▪ Advise patient to take Levodopa
01 hour before or after a meal
▪ Reduce amount of protein early
in the day, main protein meal in
the evening.
▪ Requirement: 0.7gm/Kg BW
▪ Precise amount of Vitamin
supplementation
Rehabilitation
34
Rehabilitative Mx
Gastrointestinal
Problems
Constipation:
-Altered sympathetic
innervation of the GIT,
-Concomitant
medications,
-overall limited mobility,
-impaired hydration.
▪ Adequate hydration,
▪ Increased physical activity,
▪ High-fiber diets.
▪ use of a daily osmotic agent
(lactulose)
Rehabilitation
35
Rehabilitative Mx
Bladder Problems
Detrusor Hyperreflexia
-Nocturia
-Urgency
-Frequency
▪ Timed voiding,
▪ Peripherally acting
anticholinergics (Oxybutynin),
▪ Redistribution of fluid intake:
bulk of fluid ingestion earlier in
the day
Detrusor Hyporeflexia
-Retention of urine
▪ Intermittent
catheterization,
Rehabilitation
36
Rehabilitative Mx
Occupational Therapy
-ROM activities of upper extremity with stretching
-Fine motor coordination and training, hand dexterity
training using colored pegs or beads
-Hand cycling to help train reciprocal movements
-Rocking chair to help with mobilization
-Transfer training
37
Rehabilitative Mx
Occupational Therapy (cont.)
-Safety skills
-Adaptive equipment evaluation,
Velcro closures, raised toilet, grab bars, eating
utensils with built-up handles, and key holders
-Family training and home exercise program
38
Rehabilitative Mx
Speech Problem
▪ Deep breathing and diaphragmatic breathing
exercises
▪ Articulatory speech training for dysarthria
▪ Facial, oral, and lingual muscle exercises
▪ Swallowing evaluation, including a modified
barium swallow as needed
▪ Teaching compensatory strategies for safer
swallowing
39
Thank You
40
Q & A
41

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Parkinson's Disease Rehabilitation.pptx

  • 1. Rehabilitation of a person with Parkinson’s Disease Dr. Md. Mamunul Abedin MBBS, BCS (Health), FCPS Trainee (PMR) Dept. of Physical Medicine & Rehabilitation National Institute of Neurosciences and Hospital, Dhaka 1
  • 2. Parkinson’s Disease Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately dopaminergic neurons in a specific area of the brain called substantia nigra. 2
  • 3. Epidemiology -The 2nd commonest neurodegenerative disease. -Affects men and women of all races, all occupations, and all countries. -Mean age of onset is about 60 years. Frequency increases with aging. -The prevalence of the disease will be dramatically increased in the next several decades. 3
  • 4. Etiology -Unknown (85 – 90%) -Environmental Factors Exposure to Pesticides Rural Living Drinking Well water MPTP Reduced risk with Cigarette smoking & Caffeine -Genetic Factors Gene mutations Gene associations 4
  • 5. Pathophysiology The Pathological Hallmarks of PD: -Depletion of the pigmented dopaminergic neurons in the substantia nigra -The presence of α-synuclein and other protein inclusions in nigral cells (Lewy bodies) -There are also other neuronal degenerations. Loss of dopaminergic neurotransmission: Causes motor symtomps 5
  • 6. Pathophysiology (cont.) Physiologically, Substantial Nigra is the major output region of the Basal ganglia. The output of Basal Ganglia provides inhibitory tone to Thalamus & Brainstem, and in turn, control motor functions,behavioral, emotional & cognitive functions. Decreased neuronal activity in SN is associated with movement facilitation via Dopaminergic projections. 6
  • 7. Pathophysiology (cont.) In PD, Dopamine denervation/ Loss of Dopamine tone Excessive inhibition of the Thalamus Reduced activation of Cortical motor systems Development of Parkinsonian features 7
  • 8. Cardinal Features Clinically, Parkinson’s Disease is characterized by: -Rest Tremor, -Rigidity, -Bradykinesia (Slowing), and -Gait Impairment. 8
  • 9. Clinical Features (Motor symptoms) Positive Phenomena ▪ Tremor  Resting Tremor  Postural Tremor  Re-emergent Tremor -Suppressed by sleep and activity, -Increased by fatigue or stress. 9
  • 10. Clinical Features (Motor symptoms) Positive Phenomena ▪ Rigidity  Cogwheel type  Lead pipe type ▪ Flexed Posture Dominance of progravity flexor muscles 10
  • 11. Clinical Features (Motor symptoms) Negative Phenomena ▪ Bradykinesia -Slowness of movement ▪ Loss of postural reflexes ▪ Postural instability ▪ Freezing phenomenon -Transient inability to move. 11
  • 12. Gait ▪ Slow to start walking ▪ Rapid, Short stride length, Tendency to shorten (Festination) ▪ Reduction of arm swing ▪ Impaired balance on turning Clinical Features (Motor symptoms) 12
  • 13. Normal Findings Power, Deep tendon reflexes, Plantar Eye movements Sensory & Cerebellar examination Clinical Features 13
  • 14. Clinical Features (Other Motor features) ▪ Micrographia ▪ Masked facies (Hypomimia) ▪ Reduced eye Blinking ▪ Soft voice (Hypophonia) ▪ Dysphagia 14
  • 15. Clinical Features (Non-motor Symptoms) ▪ Cognitive Impairment (Dementia) ▪ Neuropsychiatric Features: Anxiety, Depression, Apathy, Hallucinations/ Psychosis ▪ Sleep Disturbances & Hypersomnolence ▪ Fatigue, Drooling, Weight loss ▪ Sensory Disturbances (Pain) 15
  • 16. Clinical Features (Non-motor Symptoms) Autonomic Disturbances ▪ Orthostatic Hypotension ▪ Sphincter Disturbance ▪ Constipation ▪ Sexual Problems Erectile failure, Loss of Libido, Hypersexuality 16
  • 17. Differential Diagnosis  Dementia with Lewy Bodies  Multiple-System Atrophy (MSA)  Progressive Supranuclear Palsy  Secondary Parkinsonism ▪ Drugs ▪ Stroke ▪ Toxin  Wilson’s Disease  Huntington’s Disease 17
  • 18. Investigation Diagnosis is Clinical. Structural imaging is normal. Functional dopaminergic imaging is abnormal in early stages (SPECT or PET) To exclude Huntington’s/ Wilson’s disease (in younger patients) 18
  • 19. Management Drug Therapy ▪ Levodopa ▪ Dopamine receptor agonists ▪ MAOI-B inhibitors ▪ COMT inhibitors ▪ Amantadine ▪ Anticholinergic drugs 19
  • 20. Management (cont.) Surgery Deep Brain Stimulation Rehabilitation ▪ Physiotherapy ▪ Occupational therapy ▪ Speech therapy 20
  • 21. Rehabilitative Mx Medical and Nursing ▪ Use of Firm bed ▪ Regular meals with proper diet (Low Protein) ▪ Measure vital capacity and enforce incentive spirometry ▪ Gradual changing of positions, elastic stockings, abdominal binder, sodium tablets, and possibly pseudoephedrine, midodrine, and/or fludrocortisone for orthostasis 21
  • 22. Rehabilitative Mx Medical and Nursing(cont.) Bowel program for gastrointestinal hypomobility (stool softeners, bulk-forming agents, cisapride, and suppositories may be required) Bladder evaluation and urodynamics; anticholinergics (e.g., oxybutynin chloride [Ditropan]) for hyperreflexic bladder Artificial tears for lack of blinking Sexual dysfunction evaluation Anticholinergic medications before mealtime to help facilitate oral and pharyngeal movements 22
  • 23. Rehabilitative Mx Gait Disturbances ▪ Shuffling gait pattern: Decreased step and stride length, decreased cadence and velocity ▪ Festination ▪ Stooped (flexed) posture ▪ Freezing, “start hesitation” ▪ “Cautious” gait (fear of falling) ▪ Impaired balance and unsteadiness due to lightheadedness ▪ Dystonia, dyskinesia 23
  • 24. Rehabilitative Mx ▪ Relaxation techniques ▪ Slow rhythmic rotational movements ▪ Gentle ROM and stretching exercises, quadriceps and hip extensor isometric exercises ▪ Neck and trunk rotation exercises ▪ Back extension exercises and pelvic tilt ▪ Proper sitting and postural control (static and dynamic); emphasize whole body movements ▪ Breathing exercises ▪ Functional mobility training, including bed mobility, transfer training, and learning to rise out of a chair by rocking; may require a chair lift Rehabilitation for Gait Dysfunction 24
  • 25. Rehabilitative Mx ▪ Functional mobility training: Bed mobility, Transfer training, Learning to rise out of a chair by rocking; chair lift ▪ Stationary bicycle ▪ Training in rhythmic pattern to music or with auditory cues ▪ Standing or balancing in parallel bars (static and dynamic) with weight shifting, ball throwing Rehabilitation for Gait Dysfunction (cont.) 25
  • 26. Rehabilitative Mx ▪ Slowly progressive ambulation training Large steps using blocks to have patients lift legs, Proper heel-to-toe gait patterns, Feet 12–15 in. apart, arm swing; Use inverted walking stick, colored squares, or stripes as visual aids ▪ Use of assistive devices (may need a weighted walker) ▪ Aerobic conditioning (swimming, walking, cycling) ▪ Frequent rest periods Rehabilitation for Gait Dysfunction (cont.) 26
  • 27. Rehabilitative Mx Movement Initiation -Slow movement initiation. -Result from delayed activation of the motor cortex, impeding one’s ability to initiate and execute normal movement. -exacerbated with high- complexity tasks. -Difficulty in handwriting. ▪ It may be a strategy to facilitate motor tasks. ▪ Rehabilitation 27
  • 28. Rehabilitative Mx Dyskinesia -the excessive movement of muscles in the trunk or limbs that cannot be controlled voluntarily. -complication of levodopa therapy after 7 or 8 years. -due to highest conc of Levodopa, and progressive loss of dopamine neurons. ▪ If Mild, No measures ▪ If bothersome, reduction of dose & dosage of Levodopa ▪ Add Amantadine Rehabilitation 28
  • 29. Rehabilitative Mx Dystonia -the involuntary contraction of a single muscle or multiple muscles that cause an abnormal posture, -most common site is the foot (contraction with flexion of the toes and inversion of the entire foot). -Occurs when plasma concentrations of Levodopa are at their lowest and highest ▪ If at end of dose, Ingestion of another dose. ▪ In Peak-dose dystonia, if causes focal problem, Local injection of Botulinum toxin Rehabilitation 29
  • 30. Rehabilitative Mx Orthostatic Hypotension ▪ Lifestyle modification and education -Avoid warm or hot bath / A heavy meal /Excessive straining while defecating and other tasks -Taking high-fiber diets and stool softeners ▪ Gradual changing of positions (may use Tilt table) ▪ Compression leg stockings and abdominal binders. ▪ Omit unnecessary drugs ▪ Fludrocortisone or midodrine, if needed. 30
  • 31. Rehabilitative Mx Gastrointestinal Problems Swallowing Dysfunction -Dysphagia due to loss of lingual control -Esophageal dysmotility -Hypopharyngeal Stasis -Aspiration -Deficient positioning of oesophagus ▪ Oral-motor exercise by speech pathologist ▪ Chin-Tuck Maneuver ▪ Thickened liquids Rehabilitation 31
  • 32. Rehabilitative Mx Gastrointestinal Problems Nutrition: -At risk for weight loss -Amino acids & Vit B6 hampers absorption of Levodopa. ▪ Nutritional Consultation ▪ Advise patient to take Levodopa 01 hour before or after a meal ▪ Reduce amount of protein early in the day, main protein meal in the evening. ▪ Requirement: 0.7gm/Kg BW ▪ Precise amount of Vitamin supplementation Rehabilitation 34
  • 33. Rehabilitative Mx Gastrointestinal Problems Constipation: -Altered sympathetic innervation of the GIT, -Concomitant medications, -overall limited mobility, -impaired hydration. ▪ Adequate hydration, ▪ Increased physical activity, ▪ High-fiber diets. ▪ use of a daily osmotic agent (lactulose) Rehabilitation 35
  • 34. Rehabilitative Mx Bladder Problems Detrusor Hyperreflexia -Nocturia -Urgency -Frequency ▪ Timed voiding, ▪ Peripherally acting anticholinergics (Oxybutynin), ▪ Redistribution of fluid intake: bulk of fluid ingestion earlier in the day Detrusor Hyporeflexia -Retention of urine ▪ Intermittent catheterization, Rehabilitation 36
  • 35. Rehabilitative Mx Occupational Therapy -ROM activities of upper extremity with stretching -Fine motor coordination and training, hand dexterity training using colored pegs or beads -Hand cycling to help train reciprocal movements -Rocking chair to help with mobilization -Transfer training 37
  • 36. Rehabilitative Mx Occupational Therapy (cont.) -Safety skills -Adaptive equipment evaluation, Velcro closures, raised toilet, grab bars, eating utensils with built-up handles, and key holders -Family training and home exercise program 38
  • 37. Rehabilitative Mx Speech Problem ▪ Deep breathing and diaphragmatic breathing exercises ▪ Articulatory speech training for dysarthria ▪ Facial, oral, and lingual muscle exercises ▪ Swallowing evaluation, including a modified barium swallow as needed ▪ Teaching compensatory strategies for safer swallowing 39

Editor's Notes

  1. Neuronal degeneration with inclusion body formation can also affect cholinergic neurons of the nucleus basalis, norepinephrine neurons of the locus coeruleus (LC), serotonin neurons in the raphe nuclei of the brainstem, and neurons of the olfactory system, cerebral hemispheres, spinal cord, and peripheral autonomic nervous system.
  2. All motor disorders consist of excessive motor activity (positive symptoms), functional deficits (or negative symptoms) Resting: most common • Asymmetric, (‘pill rolling’) • May affect legs, jaw and chin but not head • Intermittent, present at rest, briefly abolished by movement of limb, exacerbated by walking Postural • Present immediately on stretching out arms Re-emergent tremor • Initially no tremor on stretching arms out, rest tremor re-emerges after a few seconds
  3. Rigidity: Increase in muscle tone during passive limb movement equal through entire ROM; Flexed Posture: (bowed head, chin toward chest, kyphotic thorax, protracted shoulders, internally rotated arms, flexed elbows, knees, and hips).
  4. Bradykinesia: Slowness of movement, masked facies, decreased eye blinking, inability to move. Fatigue. Loss of postural reflexes : Tendency to fall to the side (lateral pulsion) or backward (retropulsion); sitting en bloc (collapses in the chair when attempting to sit down).
  5. SPECT or PET: but does not differentiate between the different forms of degenerative parkinsonism and so is not specific for PD.
  6. DBS: Various targets have been identified, including the thalamus (only effective for tremor), globus pallidus and subthalamic nucleus.
  7. Protein seems to interfere with Levodopa absorption. So, (1) Person may benefit taking medication 30-60min before meal, (2) low protein snack during taking the dose may help with side effects of levodopa. Protein redistribution: Reduce amount of protein early in the day, main protein meal in the evening. Requirement: 0.7 gm/Kg body wt.