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8/14/2019 Recognizing the Impacts of Poliomyelitis in Children and Planning the Rehabilitation Strategies
http://slidepdf.com/reader/full/recognizing-the-impacts-of-poliomyelitis-in-children-and-planning-the-rehabilitation 1/97
RECOGNIZING THE IMPACTS OF
POLIOMYELITIS IN CHILDREN ANDPLANNING THE REHABILITATION
SRATEGIES
Ronald E. Pakasi, MD
Physical Medicine & Rehabilitation Dept.
Jakarta, Indonesia
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8/14/2019 Recognizing the Impacts of Poliomyelitis in Children and Planning the Rehabilitation Strategies
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History
• First recorded symptomssimilar to poliomyelitis:Egyptian stele datingfrom the EighteenthDynasty (1580-1350
B.C.)⇒”a crippled young man,
apparently a priest,with a withered &shortened left leg, witha foot positioned typicalof flaccid paralysis,
using his staff forsupport”
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Polio - Timeline
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Epidemiology
• Indonesia: 2
outbreaks in the
past decade
• 1995
• 2005
• Any ages:
neonates > severe
• M : F ratio = 1 : 1
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Etiology - The Virus -
• Picornaviridae(enterovirus) - RNA virus
• Enterically infecting virus• Food- / water-borne
• Fecal-oral / oral–oral /
respiratory transmission
• Initial replication:
oropharynx• Main invasion site: small
intestine
• Best temp.: 370 C
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8/14/2019 Recognizing the Impacts of Poliomyelitis in Children and Planning the Rehabilitation Strategies
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Etiology – The Vaccine -
The Vaccine • Sabin-live oral polio
vaccine (OPV)
• Widely used in 3rd worldcountries
• Vaccine-associatedparalytic poliomyelitis
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Pathophysiology
• Replication of 1 cycle: + 8hours
• RNA core: capsid proteins → allows binding to specific cellmembrane components
(gateway)• 1 hour post infection (PI):
margination of chromatin
(accumulate within thenuclear envelope)
• 2.5 – 3 hours PI: membranous
vesicles emerge → spreadoutward
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Pathophysiology
• Replication (pharynx ⇒
small intestine): first 1-3
weeks of incubation• Incubation: host-to-host
transmission possible
• Replication detectable:
24-72 hours after virus
ingestion• ± 5% pts: nervous system
involvement
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P l ti
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Paralytic Poliomyelitis
• Spinal poliomyelitis
• Bulbar poliomyelitis• Bulbospinal
poliomyelitis• Polioencephalitis
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Paralyt ic Pol iomyel i t is
• 2-5% of polioviral infection cases
• Spinal cord anterior horn cells & othermotor neurons: selectively susceptible
• Incubation: 4-10 days ⇒ may extend to 4-
5 weeks
• 1st symptoms: nonspecific fever & muscle
weakness (↓↓ >2-3 days)
• Abrupt onset of asymmetric flaccid
paralysis
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Spinal Pol iomyel i t is
• Affects LE > UE > Trunk
• Preceded by: ↑↑ muscle pain & spasm
• Paralysis: asymmetric, flaccid, patchy, proximal > distal⇒ may extent to other limbs after > 5–6 days
• Paralysis⇒ max in 48 hrs (some: > 1 wk)• Paralysis progression: ↓↓ if the fever (-) in 48 hrs
• Reflexes ↓↓ ⇒ (-) & bulbar involvement may follow
• Muscle atrophy: > 3 wks (max 12-15 wks ⇒ permanent)• Paresthesia: frequent w/o sensory dist.
• Rare accompanying conditions: trans. myelitis +
paraparesis, urinary ret., sensory & autonomic dist.
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Bulbar Pol iomyel i t is
• A.K.A. brainstem poliomyelitis (10-15% of paralyticpoliomyelitis cases)
• Isolated bulbar w/o limb weakness: more commonin children (especially w/ history of tonsils &adenoids removal)
• Adult type: bulbospinal poliomyelitis
• Pain, nuchal rigidity & hypertonia: brainstem,spinal ganglia, & posterior column
• Cranial nerves: VII, IX, X, (rare: III)⇒ facialweakness, dysphagia, dysphonia, & oculomotor
palsy (rare)
• Reticular formation: cardiorespiratory problems(discussed later)
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Polioencephalitis
• Very rare & uncommonly occurs w/o paralysis
• Paralysis: may emerges 24-48 hrs > initial onset• Clinical manifestations: tremulousness,
obtundation, agitation, & autonomic dysfunction
• Autonomic: labile hypertension / hypotension,tachycardia, arrhythmias, & hyperhydrosis
• UMN signs: spasticity, hyperreflexia, & Babinski• Other signs: muscle pains, muscle cramps,
fasciculation, & radicular pain
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Diagnostic Procedures
• Lab: CSF (pleocytosis, ↑
protein level)
• Lab: CBC, culture (stool, blood, etc.)
• EMG
• MRI
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FUNCTIONAL ALTERATIONS
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Neuromusculoskelet al Funct ion
AFP in polio: 3 phases (“triad two”)
• 1st: acute ⇒ subacute phase (1st 2 wks⇒ 2 wks to 2 mo)
• 2nd : convalescent phase (>2 mo - 2 yrs)• 3rd : chronic / residual phase (> 2 yrs)
→ post polio condition→ → post polio syndromepost polio syndrome
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8/14/2019 Recognizing the Impacts of Poliomyelitis in Children and Planning the Rehabilitation Strategies
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Neuromusculoskelet al Funct ion
• Functional alterations : observed in mobility &
gait function• UE paralysis: major predilection site → deltoids
& triceps brachii ⇒
object manipulations may
be normal
• Accompanying symptom of pain: devastating &
may disturb other functions as well
• Pain: muscles, joints, & nerves ( >> lower back)
• Hyperesthesia ⇒ pain ↑↑
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Neuromusculoskelet al Funct ion
• Children PE: transitional mobility activities& walking activity
• Tests: standing on toes, standing on heels,squat-to-stand test, sit-to-stand test, jump
in one leg, & walk test• Infants PE: observe behavior on supineposition
• Paralysis: frog-leg position
• Other tests: sharp stimulus test &
pendulum test
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Musculoskelet al Compl icat ions
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Musculoskelet al Compl icat ions
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Musculoskelet al Compl icat ions
Chi ldren wit h pol io: are st i l l in t hei r development al & growing age !!
Impact s of paralysis on a growing l imb:
• shortening & ↓↓ in diameter of the bone, due to:
• << muscle pull + vascular supply disturbance + ↓↓ nervestimulation
• Bone will become << compact & may not able tosupport loading
• Fractures may easily develop
• Bone-shortening in LE: result in LLD ⇒ disturb theposture balance on the vertebrae ⇒deformity in
vertebrae (scoliosis)
Musculoskelet al Compl icat ions
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Musculoskelet al Compl icat ions
M l k l t l C l i t i
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Musculoskelet al Compl icat ions
M l k l t l C l i t i
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Musculoskelet al Compl icat ions
Musculoskelet al Compl icat ions
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Musculoskelet al Compl icat ions
Musculoskelet al Compl icat ions
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Musculoskelet al Compl icat ions
C di l F t i
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Cardiopulmonary Funct ion
• Respiratory function → triple threat:weak respiratory muscles, poor cough
efforts & risk of food aspiration• Intercostal paralysis: AHC infection in
thoracic region
• Diaphragm paralysis: AHC infection in themid-cervical region
• Involvements in: dorsal nuclei of theVagus & the medial reticular nuclei(vasomotor nuclei): pulmonary edema,
CO2 retention, and papilledema
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Cardiopulmonary Funct ion
• Involvement of N. Vagus: dysphagia ⇒ damaged
innervation to the larynx ⇒ potential airwayobstruction (early tracheotomy
• Paralysis of the larynx: saliva / mucus go down
to the lower respiratory tract ⇒ pulmonaryinfection / edema
• Paralysis of the soft palate: speech disturbance
• Medullary / hypothalamus involvements: 2nd
hypertension
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Behavioral Problems
• Tendencies in polio survivors: develop
behavioral changes• Type A personality: non-compliant to
rehabilitation program, especially vocational
• Characteristic: hard-driving and excessiveworker, pressured, easily angered,
perfectionist, too sensitive to criticism &
failure, hyperactive; have a chronic insecurity
feeling, & low self-esteem
GENERAL REHABILITATION
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GENERAL REHABILITATION
MANAGEMENT IN POLIOMYELITIS
•ACUTE PHASE
•CONVALESCENT PHASE•RESIDUAL PHASE
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ACUTE PHASE
• Physiatrist: determine whether there are
any bulbar involvements or not• Respiratory assistance ? (life-saving
intervention)
• Infants with respiratory failure : negative
extrathoracic pressure ventilation (NEPV)
• Older children: intubation / intermittent
positive pressure ventilation
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ACUTE PHASE
• Bulbar involvement: inability of the
patient to swallow (“drown” in his/herown secretions)
• Management: respiratory assistance +positioning technique
Respi rat ory Assist ance + Posi t ioning
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Respi rat ory Assist ance + Posi t ioning
Technique
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ACUTE PHASE
• Bulbar palsy w/o respiratory failure: risk
of aspiration (+) ⇒ owing to dysphagia• Emergency management: posturing
technique using a medially-angulated bed+ pillows to support the center of the
mattress
• Secretions will trickle down from the
patient’s mouth ⇒ aspiration risk can be
prevented
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ACUTE PHASE
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ACUTE PHASE
Other rehabilitation
strategies:
• preventing
complications
secondary toprolonged bed rest /
immobilization
• pain management
ACUTE PHASE P i M
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ACUTE PHASE – Pain Management
Medications and supported by physical
modalities:• TENS
• Hot pack (Canny pack)• Infra red therapy
• Electrical stimulation
ACUTE PHASE E l M bi l i i
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ACUTE PHASE – Ear ly Mobi l izat ion
Goals of ear ly mobi l izat ion:
• maintaining & exercising movementcoordination
• preventing pressure ulcers• prevention of deconditioning syndrome
⇒ (takes place after the febrile (-) &
progression of paralysis ↓↓)
ACUTE PHASE E l M bi l i t i
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ACUTE PHASE – Ear ly Mobi l izat ion
• Bed mobilization: rolling, side-lying,
prone, sitting, or standing – using tiltingtable
• Crawling activity: if possible• Abdominal breathing exercise + chest
expansion exercise: as early as possible
• Sitting balance exercise: if possible
(preparation for ambulation)
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CONVALESCENT CONVALESCENT
PHASE PHASE
CONVALESCENT PHASE
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CONVALESCENT PHASE
• Hydrotherapy
• Muscle strengthening exercise (affected& unaffected limbs)
• Standing & gait preparation• Lower orthosis / spinal orthosis
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CONVALESCENT PHASE
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RESIDUAL PHASE
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RESIDUAL PHASE
Hallmark of rehabilitation: develop substitutionpattern of the muscles (enabling patient to
perform ADLs maximally)• Orthosis: mandatory (exc. complete recovery)
• Operative management: sometimes necessary
Evaluation of the patient:
• 1st 2 months: every week (mo-1) & every 2weeks (mo-2)
• > 2-6 months: evaluate every 2 months
• > 2 – 3 years: evaluate every 6 months
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PART II
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PART IIPART II
POSTPOST--
REHABILITATIONREHABILITATION
MANAGEMENTMANAGEMENT
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AN APPROACH TO THE PATIENT WITH
SUSPECTED POST POLIO SYNDROME
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SUSPECTED POST POLIO SYNDROME
PRIME SYMPTOMS
• Fatigue, pain, & weakness: almost alwayspresent
• Fatigue (89%); pain in muscle / joint (86%);
new weakness (83%) in previously symptomatic(69%) / asymptomatic (50%) muscles
• New Atrophy (28%) ⇒~ Post Polio Muscular
Atrophy (PPMA)• ADL difficulties (78%) = functional loss
⇒
walking (64%); climbing stairs (61%);
dressing (17%)
ADDITIONAL PRESENTING PROBLEMS
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ADDITIONAL PRESENTING PROBLEMS
• Pulmonary dysfunction
• Sleep Disorders• Dysphagia
• Cold intolerance• Degenerative arthritis
• Social and psychological problems
IDENTIFY AREAS OF DYSFUNCTION
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• History ⇒ identifying: fatigue, dysphagia, sleepdisorders, & ADL alterations
• Neurologic exam: atrophy / weakness, reflexesare not ↑↑
• Observe the "good" l imb : (+) significant
weakness w/o patient’s awareness• Leg muscles: use functional tests [MMT may notdetect ↓↓ quadriceps strength to 30% of normal→ although sufficient for routine ADLs]
• MMT: use mechanical advantage ⇒ (e.g. mm.triceps / quadriceps with the elbow / knee
flexed >900
; m. psoas in supine position)
IDENTIFY AREAS OF DYSFUNCTION
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IDENTIFY AREAS OF DYSFUNCTION
• General PE & biomechanical exam: note
obesity, joint deformity, overusesyndromes, & scoliosis
• EMG: document previous AHC disease
(especially if previous polio is doubtful) &
ruling out other neuromuscular pathologies
/ identifying subclinically involved muscles• Lab: CK ↑ (may not correlate with
progressive weakness)
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REHABILITATION
STRATEGIES
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Management of PPS
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Management of PPS
3. Management of fatigue
• Energy conservation techniques• Lifestyle changes
• Pacing• Regular rest periods, naps during day
• Meds: amitriptyline (improve sleep) /pyridostigmine (?? ⇒ trial in progress)
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Management of PPS
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4. Management of pain
A. Post-polio muscular pain, muscular cramps,
muscular pain with activity• Activity reduction
• Pacing (rest periods during activity)
• Moist heat, ice, and stretching• Use of assistive devices
• Life style modifications
B. Fibromyalgia
• Meds: amitriptyline / cyclobenzaprine
• Aerobic exercise
Management of PPS
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4. Management of pain
C. Joint and soft tissue abnormalities
• Modification of extremity use• Physiotherapy for use of physical modalities,
strengthening, stretching.
• Orthoses / other assistive devices
• Meds: NSAIDs, steroid injections / Surgery
D. Treatment of other superimposed neurologicdisorders (e.g. CTS, radiculopathy, spinal
stenosis)
Management of PPS
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g
5. Pulmonary dysfunction
• Preventive measures (pneumococcalvaccine, yearly influenza vaccine)
• Ventilatory assistance (non-invasive
methods preferred)
• Identification & treatment of sleep apnea
• Glossopharyngeal breathing
Management of PPS
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g
6. Dysphagia
• Changing or restricting diet• Use of special breathing techniques
• Use of special swallowing techniques• Monitoring fatigue, & taking larger meals
earlier, & smaller meals later• Avoiding eating when fatigued
Management of PPS
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g
7. Psychosocial difficulties
• Interdisciplinary approach• Post-polio support group
• Evaluation and treatment by socialworkers, psychologists, psychiatrists
Lifestyle Modifications
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• The "sine qua non" of all attempts atsuccessful management of PPS
• Patients: desperate, have a belief toovercome their disability through the "no pain, no gain" approach
• “No pain, no gain“ approach: may besuccessful after the acute onset ⇒ now
become self destructive• Persistence in this approach: spiral of
deteriorating function & ↓↓
self worth
Lifestyle Modifications
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• Understand the concept of "living with"
PPS !!
• Understanding the need for lifestyle
modification: rarely achieved at 1st visit→ must be reintroduced by an OT/PT and
reinforced & monitored at subsequentphysician visits
Increase Muscle Capacity
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a) Achieving ↑↑ strength / endurance
• Strength: isometric exercise ⇒selectmuscles carefully (some muscles will
already be functioning at their maximum)
• Exercise: may have a deleterious effect
by forcing these muscles beyond their
metabolic capacity & producing injury
Increase Muscle Capacity
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b) Appropriate exercise: ↑↑ endurance, ↓↓susceptibility to fatigue, ↓↓ long term
deterioration• Initial difficulties: occur in almost allpatients (from overdoing?)
• May tend to associate fatiguing ADLs(challenge the weakest musculature & do
not provide an effective aerobic traininglevel) with exercise
⇒
can be an instructive opportunity for
understanding the “lifestyle modification"
Goals in aerobic exercise:
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– Educate the patient to avoid potentiallyharmful exercise-induced fatigue
⇒ Strategy: establish the level of peakperformance by patient history → start at50% of peak performance & slowly ↑↑
performance as tolerated– Select exercises which can create a training
effect in the patient with weakened,atrophic musculature & overuse syndromes
⇒ Strategy: exercise intervals withintervening rests, just as is pacing of ADLs
Increase Muscle Capacity
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c) Use of bracing, orthotics, or other aids which extend,amplify or substitute for muscles (to ↑ musclecapacity)
d) Pharmacologic treatment of fatigue: (↑↑ fatiguethreshold) ⇒ still observed & needs confirmation:
– Amantadine: up to 100 mg BID as tolerated
– Deprenyl: up to 5 mg BID as tolerated
– Mestinon: up to 60 mg TID (needs carefulmonitoring!)
Medications: just the aids to give a running start forthe rehabilitation process (patient shouldunderstands them as a non curative treatment)
Decrease Muscle Load To LessThan Muscle Capacity
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a) PACING of activity
• Implementation: patients must identify each of
the ADL’s length of time (before experiencingfatigue)
• Break up activities into smaller modules of time(each with << duration (before fatigue occurs)
• Concept of PACING: ENERGY BUDGETINGENERGY BUDGETING ⇒ patient has a fixed energy expenditure (EE) foreach day & should be "spent" on the highest
priority of ADLs• Concept of exceeding use of this daily limit:
acquire debt ⇒
correlates to metabolic injury of
the motor unit (overuse)
Decrease Muscle Load To Less
Than Muscle Capacity
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p y
b) Other means of decreasing muscle load:
• diet (for overweight >>)• orthotics (improve mechanical efficiency)
• wheelchairs / scooters to save EE• treatment of chronic overuse syndromes
Treat Specific Complications
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• a) Attention to specific complications: e.g. dysphagia,pulmonary dysfunction & sleep disturbances
• b) Functional consequences resulting from overusesyndromes (⇒ joint deformity)
→ Physiatry consultation / orthopedic intervention
→ Orthotic prescriptions (i.e., splints, braces, AFO's)• c) Somatization, depression, anxiety, & self worth
problems: may occur as capacity ↓↓ (referral forcounseling or polio support group)
• d) Evaluate and/or modify work duties through referralto OT or vocational counselor
Exercise in PPS Patients
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• Include: isotonic, isokinetic and isometricstrengthening exercise programs + aerobic
exercise• Average level of aerobic fitness in post-polio
patients: 5.6 METS (similar to MCI patients)
• Aerobic exercise (UE + LE): bicycle ergometeror treadmill
• Bicycle ergometer: improved VO2max, duration
of exercise, watts attained during exercise, andmaximum expired volume per unit time
• Treadmill training: improved economy orenergy cost of walking (+ walking duration)
Exercise in PPS Patients
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Exercise prescription: dependent on several factors:
• Isometric: MMT < 3 or in muscles over a painful joint
• Isotonic: MMT > 3 and without a painful joint• Aerobic exercise program: bicycle ergometer, walking,
or swimming (should be an activity which the patientenjoys to increase compliance)
• Warm-up & cool-down period + stretching exercisesshould be included
• Early in the exercise program: monitored carefully (to
ensure that the exercise prescription is being followedcorrectly & muscles and joints overuse is not occurring)
• Encourage self-monitor
Exercise in PPS Patients
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Exercise in PPS Patients
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Exercise in PPS Patients
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THANK YOUTHANK YOU
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POST PRESENTATION
NOTES…
Pathophysiology of PPS
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• EXTENSIVE NEURONAL INVOLVEMENT IN
THE ACUTE POLIO INFECTION• MOTOR UNIT REMODELING IN THE POST
RECOVERY PHASE
• DECOMPENSATION THEN PRODUCES
POST POLIO SYNDROME
EXTENSIVE NEURONAL INVOLVEMENT IN THE ACUTE POLIO INFECTION
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• Infection is >> widespread than anterior horn cells (AHC)
• AHC infection: largely subclinical (⇒ residual capacity of uninfected & surviving neurons)
• Infection outside AHC: largely subclinical (may contributeto the disabling symptoms of fatigue & pain ⇒ physiologic basis is uncertain)
• 95% of motor neurons: infected in an average acuteinfection (50% neuronal fatality rate)
• Segmental involvement ↑↑ ( causing lack of weaknesssymmetry)
• Other involvements: intermediolateral horns & dorsal rootganglia, motor cortex, hypothalamus, globus pallidus,brainstem nuclei, reticular formation, cerebellar roof
nuclei, & vermis.
MOTOR UNIT REMODELING IN THE POST
RECOVERY PHASE
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RECOVERY PHASE
• Example of muscles: quadriceps (N) has ± 200 musclefibers/ AHC {AHC (N) can adopt ± 1,000 orphanedmuscle fibers}
• > 50 % motor units may be lost w/o symptoms
(Walking (N): only 15-20% of max muscle strength)• Clinical improvement: through recovery of mildly
affected neurons, collateral sprouting, &
strengthening (hypertrophy) of intact musculature• ↑↑ demand on surviving motor units: ⇒ ↑↑ firing
frequency ⇒ change in fiber type to predominantlyaerobic "slow twitch" fibers with ↑↑
vascularity
DECOMPENSATION THEN PRODUCES POST POLIO SYNDROME
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• ↑↑ metabolic burden on surviving AHC (includingasymptomatic muscles) as they direct more muscle
fibers to contract→ often to achieve the same forceof contraction
• ⇒⇒ AHC fatigue ⇒⇒ premature metabolic injury(even cell loss)
• Fatigued neurons: unable to continue to trophicallysupport as many muscle fibers ⇒⇒ collateral sproutsto some muscle fibers will degenerate ⇒⇒ strength
will be lost to the motor unit ⇒⇒ spiral of decline !!• This mode of decompensation (+ fatigue) ⇒ AHC
based (not a static process → may be dynamicdenervation & reinnervation)
DECOMPENSATION THEN PRODUCES POST POLIO SYNDROME
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Anot her mode of decompensat ion is muscle f iber based
• Rapidly firing muscle fibers ⇒⇒ ↑
lactic acid (not be
adequately dissipated) ⇒ especially true withisometric contraction ⇒ muscle fiber fatigue ⇒⇒muscle fiber injury ⇒ lost function ⇒ spiral of decline !!
• ↑↑ mechanical load (e.g. from ↑↑ weight or ↑↑ physical activity) or ↓↓
force generating capacity
(e.g. from inactivity following illness / injury) ⇒⇒met abol ic f ailure in motor units / muscle fibersfunctioning close to their capacity
DECOMPENSATION THEN PRODUCES POST POLIO SYNDROME
Th l i l i k j i &
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• The resulting relative weakness ⇒⇒ joint &muscle misuse & overuse ⇒⇒ arthritis &overuse syndromes
Cent ral fat igue may also be a fact or
• Polio virus infection of the motor strip & thereticular activating system
• Definition: "Increased mental effort
necessary t o per form a f ixed amount of muscle cont ract ion“
• PPS patients: feelings of fatigue (many report
hitting a "post polio wall")
Pulmonary Dysfunct ion
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• Weakness of the breathing muscles (i.e. diaphragm &ribcage
• May cause: dyspnea on exertion (& at rest), poorclearance of respiratory secretions → ↑↑ risk of pneumonia, & ↑↑ resting arterial CO2 level
• Pulmonary function tests: restrictive pattern (small lungvolumes) → neuromuscular weakness based
• Mechanical ventilation may be required (very severecases)
⇒ small mechanical ventilators → deliver breathsthrough a comfortable plastic nose mask (performedwhile the patient is asleep at night ⇒ improved daytimefunction)
Sleep Disorders
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• ↑↑ incidence of sleep disturbances + poor sleepquality & frequent awakenings
• Most important etiologies must be ruled out:central, obstructive & mixed sleep apneas
• Nocturnal hypoxemia & hypercarbia ⇒⇒
worsen the daytime function of the breathingmuscles
• Management: nocturnal non invasive ventilation
→ improve sleep quality & ↓↓ symptoms of daytime sleepiness (may also improve daytimerespiratory muscle function)
Dysphagia
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• Eating / swallowing disturbances: more common inbulbar polio patients
• Evaluation: video fluoroscopy (pharyngeal const r ict or weakness )
• Laryngeal penetration & loss of the cough reflex: maybe asymptomatic ⇒
an underestimation of the
presence & severity of dysphagia (?)
• Patients may have already employed compensation(e.g. altering diet, cutting solids into small pieces,
chewing it thoroughly, taking small sips of liquids,eating slowly, & using postural maneuvers)
• Frequent accompanying conditions: progressive speechdifficulty (e.g. ↑↑ hoarseness, weakness, slurring)
Cold int olerance
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• Occurs in ± 29% cases
• Limbs may be cold ⇒ cold exposureproduces weakness
• Involvement in the intermediolateral
column (?) ⇒⇒ vasoparesis, venous
pooling, & excessive heat loss
PAST HISTORY OF PPS
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• Average age of polio onset: 7 yr
• Median time to max. recovery: 8 yr
• Median period of stable neurologic & functionalstatus: 25 yr
• Median post polio symptom duration before patient
presents for evaluation: 5 yr• Variables associated with shorter interval to PPS:greater severity & greater age.
• Initial symptoms: most freq. in LE →
affected in
acute illness ⇒ (UE weakness is easier to compensatew/o resulting in overuse)
• Onset: usually insidious (frequently precipitated by
injury, illness, bed rest, or weight gain)