Rehabilitation of a person with Parkinson's Disease. There is a brief discussion about Parkinsons disease, Etiology, Pathology, Pathogenesis, Clinical Features, Medical Management, Physiatric and Rehabilitative Management as well. Hope a medical personnel especially Physical Medicine Residents will be benefitted from this.
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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
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
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
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
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
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
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.
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
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).
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).
SPECT or PET: but does not differentiate between the different forms of degenerative parkinsonism and so is not specific for PD.
DBS: Various targets have been identified, including the thalamus (only effective for tremor), globus pallidus and subthalamic nucleus.
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.