Post polio syndrome is characterized by new muscle weakness, fatigue, and pain in polio survivors decades after their initial bout of polio. It is believed to be caused by overwork of motor neurons that survived the initial poliovirus infection but were left vulnerable. As time passes, these neurons fatigue and can no longer sufficiently innervate muscles. Treatment focuses on managing new symptoms, preserving function through exercise and assistive devices, and addressing pain. Physiotherapy plays a key role through energy conservation techniques, strengthening, and physical modalities like heat.

1. POST POLIO SYNDROME
• Following the acute illness and a period of rehabilitation, polio
patients eventually reached a plateau of neurological and
functional recovery that was believed to remain essentially static
• However, research shows that over one half of the survivors of
paralytic polio experience new health problems related to their
original illness in about 30 to 50 years after their initial polio and
include new weakness, fatigue, pain, and functional loss.

2. DEFINITION OF POST POLIO SYNDROME
• An otherwise unexplained constellation of symptoms which may
include weakness, fatigue, pain, heat or cold intolerance, and
swallowing, breathing, or sleep disturbance developing in a
patient who had paralytic polio.
• Post Polio Muscle Atrophy (PPMA) has been used as the label for
the above symptoms when they include progressive muscle
atrophy
• The cardinal symptom is new weakness

4. A prior episode of paralytic polio confirmed by
history, physical exam, and typical findings on EMG
• Documented history of polio (acute, febrile illness producing
motor but no sensory loss)
• Noting whether other members of the patient’s family or
neighbors had a similar illness
• Characteristic feature - focal, asymmetric weakness, and/or
atrophy on examination

5. Standard EMG evaluation demonstrates
changes consistent with prior AHCD
• Increased amplitude and duration of motor unit action potentials
• Increased percentage of polyphasic potentials
• In weak muscles, a decrease in the number of motor units on
maximum recruitment
• Fibrillations and sharp waves may or may not be present

6. A period of neurologic recovery followed by an
extended interval of neurological and functional
stability preceding the onset of new problems
• Interval of neurologic and functional stability usually lasts 20 or
more years
• Characteristic pattern of recovery - three stages
(1) paralytic polio in childhood or later in life
(2) partial to fairly complete neurologic and functional recovery
(3) a period of functional and neurologic stability lasting many years
(4) the onset of new health problems

7. Gradual or abrupt onset of new neurogenic,
nondisuse weakness in previously affected and/or
unaffected muscles
• May or may not be accompanied by other new health problems
such as excessive fatigue, muscle pain, joint pain, decreased
endurance, decreased function, and atrophy
• New neurogenic weakness is essential for making the diagnosis

8. Exclusion of medical, orthopedic, and neurologic
conditions that might cause the health problems
listed above
• Often the most difficult to establish
• chronic illnesses, diseases, or psychiatric disturbances that afflict
the general population might affect polio patients as well
• Similar set of overlapping signs and symptoms may occur.
• Eg. Compression neuropathies, radiculopathies, degenerative
arthritis, disc disease, obesity, anemia, diabetes, thyroid disease,
and depression

9. Proposed Etiologies of Post-Polio Syndrome
Motor unit dysfunction due to overuse or premature aging of large motor units.
Musculoskeletal overuse
Musculoskeletal disuse
Chronic polio virus infection or virus reactivation
Motor neuron degeneration (glial, vascular, and lymphatic changes caused by acute polio)
Loss of motor units with normal aging
An immune mediated syndrome

10. Motor Unit Dysfunction Due to Overwork or
Premature Aging of Polio Affected Motor Units
• Most widely accepted theory is that of neuron fatigue
• The original viral attack of the anterior horn cells may have left
some motor neurons functional but impaired, making them more
vulnerable to dysfunction as time passes
• Abiotrophy – loss of vitality

11. Muscle Overuse
• Both Windebank et al. at the Mayo Clinic and Maynard found that
new weakness occurred more often in the weight-bearing muscles
of the legs than in the non-weight-bearing muscles of the arms.
And those limbs affected the most by the original disease were
the most susceptible to new weakness.
• Chronic mechanical strains on joints, ligaments, and soft tissues
that have not been supported well for 30 or more years

12. Muscle Disuse
• Well known that disuse leads to both deconditioning and muscle
weakness in healthy individuals
• Similarly, polio individuals have been noted to have similar short-
term increased weakness when forced to remain sedentary with
illness or injury

13. Loss of Normal Motor Units with Aging
• While anatomical and electrophysiological studies have
demonstrated that there is a loss of motor neurons with advancing
age, this becomes prominent only after 60 years of age
• A recent study by Trojan et al. demonstrates that older individuals
are more likely to develop PPS

14. Predisposition to Motor Neuron Degeneration
Due to Glial, Vascular, and Lymphatic Damage
• Some investigators have suggested - damage to the glial cells and
vascular supply at the time of infection can lead to secondary
dysfunction of AHC
• While vascular damage is sometimes seen, it is believed that this
is secondary to the severe inflammatory responses
• Most studies show that polio affects only the neural cells and not
the glial or vascular endothelial cellstherefore it is unlikely that
these changes play a large part in the clinical deterioration seen
with PPS

15. Virus Reactivation or Persistent Infection
• Animal studies have shown that poliovirus and other picornaviruses
may persist in the CNS and produce late or chronic disease
• an active controversy still exists regarding this hypothesis

16. An Immune-Mediated Syndrome
• A study by Pezeshkpour and Dalakas described what appeared to be
evidence of an ongoing inflammatory or immune response -- active
inflammatory gliosis, neuronal chromatolysis, and axonal spheroids in
the spinal cords of polio patients who died many years later of other
causes
• Steegman also found inflammatory infiltrates, including lymphocytes,
plasma cells, and macrophages in the parenchyma and perivascular
spaces in five of seven post-polio patients
• Antibodies are found that could be directed toward neurons, nerve
terminals, or postsynaptic antigens. This suggests that PPS could be an
autoimmune disorder mediated by antibodies produced in situ

18. Pathophysiology

19. Knowledge of the
pathophysiology of acute
polio is necessary to
understand the possible
causes for PPS
Poliovirus - positive single-
stranded RNA enterovirus
belonging to the
Picornavirus group
Three polio viruses, 1, 2,
and 3

20. 4-8%
Symptoms-
Low grade fever
Sore throat
Vomiting
Abdominal pain
Loss of apetite
Malaise
Recovery - Complete
1-2%
Symptoms-
Headache
Nausea
Vomiting
Pain, stiffness back and legs
Tripod sign
Kiss the knee test
Head drop sign
Neck rigidity
Recovery – within 2-10 days
0.5-1%
Phases-
Minor – same as abortive
Major – msc pain, spasm, return of fever
Followed by – rapid onset flaccid paralysis
complete within 72hrs
Rare
Symptoms-
Irritability
Delirium
Disorientation
Tremors, convulsions
UMN type paralysis
Infection
Inapparant 90-
95%
Apparent 5-10%

21. ParalyticPM
Spinal
Bulbar
BulboSpinal
Most common 80%
Results from LMN lesion of AHC
Affects muscles of legs/arms/trunk
Severe cases – Quadriplegia/paralysis
of trunk, abd, thoracic muscles
Assymetric paralysis (legs>arms)
Descending paralysis
Floppy muscles
Reflexes diminished
Sensation normal
Residual paralysis if after 60 days
2%
Life threatening
Cranial nerve lesion – vagus
SYMPTOMS-
Nasal twang, hoarseness
Nasal regurg
Dyspnoea
Dysphagia
Child refuses feed
Chances of aspiration
Involvement of resp centre – Shallow
irregular resp
Vasomotor centre
Pulse rapid weak thread
20%
Combination

22. PATHOLOGY: PHYSIOLOGIC AND CLINICAL
CONSEQUENCES
• EXTENSIVE NEURONAL INVOLVEMENT IN THE ACUTE POLIO
INFECTION -In addition to the anterior horns in the spinal cord,
infection involves intermediolateral horns and dorsal root ganglia.
Infection also involves motor cortex, hypothalamus, and globus
pallidus, brainstem nuclei, reticular formation, cerebellar roof
nuclei, and vermis
• MOTOR UNIT REMODELING IN THE POST RECOVERY PHASE -
Clinical improvement occurs acutely through recovery of mildly
affected neurons, collateral sprouting, and strengthening
(hypertrophy) of intact musculature.

23. PATHOLOGY: PHYSIOLOGIC AND CLINICAL
CONSEQUENCES
Central fatigue may also
be a factor.
• Polio virus infection of
the motor strip and the
reticular activating system
• A working definition for
central fatigue is:
"Increased mental effort
necessary to perform a
fixed amount of muscle
contraction"
Increased metabolic
burden on surviving
anterior horn cells
• fatigue
• metabolic injury
• collateral sprouts to some muscle
fibers will degenerate
• The strength of these muscle fibers
will be lost to the motor unit
Another mode of
decompensation is muscle fiber
based
• Rapidly firing muscle fibers
• more lactic acid
• may not be adequately
dissipated.
• Muscle fiber fatigue
• muscle fiber injury, lost
function, and a spiral of decline
DECOMPENSATION THEN PRODUCES POST POLIO SYNDROME

24. Diagram showing the neuromuscular effects of polio and
the PPS
Normal motor units
showing healthy
motorneurons,
their axons and the
muscle fibres they
innervate
Initial polio virus
with varying
motorneuron death
and denervation of
their muscle fibres
(dotted line)
Recovery-Axons from
surviving motor
neurons sprout
new fibres to
innervate denervated
muscle fibres
Early PPS
New loss of nerve
fibres and muscle
fibre denervation
Late PPS with
further loss of
nerve fibres and
muscle fibre
denervation

25. Residual paralysis
• Acute phase of illness lasts 0-4 weeks
• Recovery variable
• At 60 days – mild to severe residual paresis
• Max recovery – first 6 months
• Slow recovery – upto 2 yrs
• After 2 yrs – Post Polio Residual Paralysis persists

26. PRIME SYMPTOMS
• Statistical summary of the clinical characteristics of
several series of PPS patients is as follows:
1. Fatigue, Pain, and Weakness are almost always present.
Fatigue (89%); Pain in Muscle or Joint (86%); New weakness (83%)
in previously symptomatic (69%) or asymptomatic (50%) muscles.
2. New Atrophy (28%); This equates to Post Polio Muscular
Atrophy (PPMA)
3. Activities of daily living difficulties (78%) = functional loss
Walking (64%)
Climbing Stairs (61%)
Dressing (17%)

27. ADDITIONAL PRESENTING PROBLEMS
1. Pulmonary dysfunction from weakness of the respiratory muscle
2. Dysphagia - Many PPS patients reported some new difficulty with
eating or swallowing more commonly in those with bulbar polio.
Some progressive speech difficulty such as increased hoarseness,
weakness, or slurring.
3. Cold intolerance (29%) - Limbs may be cold and cold exposure
produces weakness. This is thought to be due to
intermediolateral column involvement resulting is vasoparesis,
venous pooling, and excessive heat loss
4. Degenerative arthritis - A joint that is biomechanically
disadvantaged may develop degenerative arthritis.
5. Social and psychological problems

28. PAST HISTORY
• Average age of polio onset is 7 years.
• Median period of stable neurologic and functional status is 25
years.
• Median post polio symptom duration before patient presents for
evaluation is 5 years.
• Variables associated with shorter interval to PPS: greater severity
and greater age.
• Initial symptoms are most frequent in the lower limb most
affected in the acute illness. (Upper extremity weakness is easier
to compensate for without overuse resulting.)
• The onset is usually insidious

29. ELECTRODIAGNOSTIC FEATURES
EMG in acute poliomyelitis is –
• Poor MUAP recruitment at the onset of weakness
• Followed by the development of fibrillation potentials in widespread muscle groups after 3 to 4
weeks
• Fibrillation potentials subside as reinnervation by surviving motor units proceeds during recovery.
The same is true in chronic polio.
• Some investigators report that there is an increase in muscle membrane instability between those
patients that are clinically stable (no new weakness) and those who are clinically unstable (new
weakness).
• The muscles that become extremely weak and atrophic have few to no MUAPs, but virtually all,
including clinically normal muscles, will have large, polyphasic MUAPs and abnormal, decreased
recruitment

30. Causes of Pain in the Polio Survivor

31. Post-Polio Muscle Pain
Pain in polio-affected muscles-
• May be similar to pain of acute polio -very
much like the pain pt. had with acute polio, if
they remember that
• Associated with muscle cramps, twitching, or
crawling sensation
• Often increased at night or end of day and at
rest
• Exacerbated by physical activity, stress, and
cold

32. Overuse syndromes and soft tissue pain
• Caused by injury or inflammation of soft
tissues: muscles, tendons, bursa, and
ligaments
• Strains, sprains, tendonitis, bursitis,
myofascial pain
• Overuse syndromes from the repetitive use
of mobility aids
• Often affects strong limb- Related to body
mechanics, positioning, posture

33. Biomechanical/degenerative disease pain
• Changes in normal joints due to wear and tear
• Excess stress of joints due to altered body
mechanics
• Joint deformity
• Degeneration in spine-discs, joints and
increased curvature
• Secondary nerve compressions
• If there are sensory changes, there’s something going
on in addition to post-polio changes

34. Bone pain
• Osteoporosis
• Fractures:
• Traumatic severe fracture, compound fractures and multiple
breaks
• Spontaneous

35. Comprehensive mx of
PPS
NEURO
LOGY
PHYSIATRY
PHYSICAL
THERAPY
SUPPORT
GROUPS
PULMONO
LOGY
PSYCHO
LOGY
OT
SPEECH
PATHOLOGY

36. Occupational Therapy and Post Polio
Syndrome
• Energy conservation and work simplification
• Upper limb splints and orthoses eg. mobile arm support
• Assistive technology and adaptive equipment
● toilet aids, bath/shower aids,
● handrails,
● long handled reachers,
● long handled personal care cleaning devices, and
● plate guards
• Mobility eg. assessment of mobility devices that do not include walking aids. consists of
assessment regarding the need for wheelchairs
• Environmental modifications to home area
• Vocational rehabilitation

37. Physiotherapy- Cornerstone of PPS mx
Management of New Weakness
Controversial
Early case reports (1915-1957) - exercise resulted in further damage to already
vulnerable motor units and resulted in increasing weakness
Other studies (1948-1966) - progressive resistive exercises produced improvements in
muscle strength
Guidelines -
Appropriate individualised exercise programmes
Monitore for deterioration in muscle strength, increased pain or increased fatigue
Learn to monitor and manage weakness and fatigue prior to commencing an exercise
programme
Avoid muscle overuse, manifested as an aching on exertion

38. Physiotherapy- Cornerstone of PPS mx
Management of pain
• Decrease Muscle Load To Less Than Muscle Capacity:
• PACING - break up activities into smaller modules of time, each of which is of less duration
than the time required to produce fatigue
• A corollary concept - ENERGY BUDGETING which imagines that one has a fixed expenditure
of energy for each day and that this sum should be "spent" on activities of the highest
personal priority
• Weight reduction
• Use of aids and appliances to relieve or support weak muscles and joints
• Electrophysical agents - Heat / TENS
• Stretching exercises / Strengthening exercises
• Hydrotherapy

39. The role of the Orthotist
Role is that of biomechanical back up to the clinical team.
Provides-
• Insoles
• Foot orthoses
• Ankle-foot orthoses (AFO)
• Knee ankle foot orthoses (KAFO)
• Spinal jackets

40. Pharmacological interventions
• Amantadine, bromocriptine and modafinil act on different regions
of the brain and are intended to address generalised fatigue in PPS
• Insulin-like growth factor (IGF-I) and human growth hormone,
which stimulates the secretion of IGF-I (IGF-I is thought to
enhance regeneration of peripheral nerves by axonal sprouting
which in turn positively influences muscle strength)
• Medications for the amelioration of fatigue must be understood as
aids which can give a running start to the rehabilitation process.
However, if they are perceived by the patient as a form of
curative treatment, they will only forestall the day of reckoning.

41. Thank you