introduction, historical background, history of polio vaccine, definition, epidemiology, mode of transmission, pathogenesis and its phase, clinical presentation - preparalytic and paralytic stages. acute stage, convalescent stage, recovery stage, residual stage or post polio syndrome. investigations, medical treatment, surgical management , rehabilitation

1. MRS. M.PRADEEPA MPT (NEURO)
VICE PRINICIPAL
PPG COLLEGE OF PHYSIOTHERAPY
COIMBATORE, TAMILNADU, INDIA
POLIOMYELITIS

2. Introduction
 Polio also known as poliomyelitis is a highly
contagious disease caused by a virus that attacks
the nervous system
 A major cause of paralysis and death 30 yrs ago,
now rare with the introduction of effective
vaccines and improved sanitation.

3. Prehistory
The effects of
polio have been
known
since prehistory
Egyptian paintin
gs and carvings
depict healthy
people with
withered limbs,
and children
walking with
canes at a
young age.

4. History of Polio
 The first clinical description was provided by the
English physician Michael Underwood in 1789,
where he refers to polio as "a debility of the
lower extremities"
 The work of physicians Jakob Heine in 1840
and Karl Oskar Medin in 1890 led to it being
known as Heine–Medin disease.
 The disease was later called infantile paralysis,
based on its propensity to affect children.

5. First US Polio Epidemic
 The first major documented
polio outbreak in the United
States occurred in Rutland
County, Vermont (1894).
Eighteen deaths and 132 cases
of permanent paralysis were
reported.
 Charles Caverly, MD, was one
of the first physicians to
recognize that polio could occur
with or without paralysis.

6. Contagious Nature of Polio
Discovered
 The contagious nature of
polio would be established
in 1905.
 After a series of polio
epidemics in Sweden, Ivar
Wickman (1872-1914)
published two important
findings about polio.
 First, he suggested that
polio was a contagious
disease that could be
spread from person to
person.
 Second, he recognized that
polio could be present in
people who did not appear
to have a severe form of the
disease. These cases are

7. Poliovirus Identified
 In Vienna, Karl Landsteiner, MD (1868-
1943), and Erwin Popper, MD (1879-
1955), announced that the infectious
agent in polio was a virus.
 Popper and Landsteiner deduced the viral
nature of polio by carefully filtering
preparations of spinal cord fluid from a
person who had died of polio. The filters
were known to trap bacteria. When
Popper and Landsteiner injected the
filtered preparations into monkeys, the
monkeys developed polio. The
researchers then concluded that an
infectious particle smaller than bacteria
caused the disease.
 Poliovirus itself would not be visible to

8. Flexner Investigates Polio
Immunity - 1910
 At the Rockefeller Institute for
Medical Research in New
York, Simon Flexner, MD
(1863-1946), showed that
“germicidal substances” were
present in the blood of
monkeys that had survived
polio. Other researchers
reported similar results with
humans. These substances
were neutralizing antibodies to
polio. Researchers took this
finding to indicate that a
vaccine might be used to

9. The Iron Lung - 1929
 Philip Drinker, PhD (1894-
1972), and Charles
McKhann, MD (1898-1988),
at Boston Children’s
Hospital and Harvard
published a paper
describing successful use of
an artificial respirator for
patients suffering from
paralytic polio.
 The machine, first known as
the Drinker respirator and
later as the iron lung, would
provide temporary and in
some cases, permanent
breathing support for people
suffering paralysis of the
diaphragm and intracostal
muscles, which are
essential for respiration.

10. More Than One Type of Poliovirus
Proposed – 1931 & 1949
 Australian researchers Frank M. Burnet (1899-1985)
and Jean Macnamara (1899-1968) infected monkeys
with polio from a fatal human case of the disease.
 The monkeys had recovered from a previous case of
polio and yet were paralyzed by the new infection.
 Their work showed that there was more than one type
of poliovirus, and that previous infection with one type
did not confer immunity to another type.
 The implication was clear: a polio vaccine would need
to provide protection from all types of polio.
 It would be 20 years before David Bodian and Isabel
Morgan (1949) would demonstrate that there are
three types of polioviruses.

11. Polio vaccine
 The first polio vaccine, known as inactivated
poliovirus vaccine (IPV) or Salk vaccine, was
developed in the early 1950s by American
physician Jonas Salk. This vaccine contains
killed virus and is given by injection.
 In the 1960s a second type of polio vaccine, known
as oral poliovirus vaccine (OPV) or Sabin vaccine,
named for its inventor American physician and
microbiologist Albert Sabin, was developed. OPV
contains live attenuated (weakened) virus and is
given orally.
 Vaccines, whether killed or live, may contain strains of
all three poliovirus serotypes—PV1, PV2, and PV3—
or of just one or two (serotypes are closely related
though distinguishable forms).

12. Polio in India
 The Indian Council of Medical Research (ICMR) had established a Polio
Research Unit (now Enterovirus Research Centre, EVRC) Mumbai in
1949. Data on epidemiology of urban poliomyelitis analysis were
collected by pioneers.
 The second polio research unit in India was the Enterovirus Laboratory,
established in 1964, in the Christian Medical College (CMC), Vellore,
Tamil Nadu.
 Polio immunization using imported OPV was introduced in Mumbai by
the city corporation in 1964 and in Vellore by CMC in 1965.
 Until early 1990s India was hyperendemic for polio, with an average of
500 to 1000 children getting paralysed daily.
 India, vaccination against polio started on 1978 with Expanded
Programme on Immunization (EPI). By 1999, it covered around 60% of
infants, giving three doses of OPV to each. (PULSE POLIO PROGRAM)
 The last reported cases of wild polio in India were in West Bengal and
Gujarat on 13 January 2011
 India received polio-free certification along with the entire South-East
Asia Region of WHO on 27th March 2014 by WHO

13. Etymology
 The term derives from the Ancient Greek poliós
meaning "grey“ and myelós referring to the grey
matter of the spinal cord, and the suffix -itis,
which denotes inflammation of the spinal cord's
grey matter, although a severe infection can
extend into the brainstem and even higher
structures, resulting in polioencephalitis, resulting
in inability to breathe, requiring mechanical
assistance such as an iron lung

14. Definition
 An acute viral infection in which the anterior horn
cells of the spinal cord and motor nuclei of the
brain stem are selectively involved.

15. Etiology
 The poliovirus is a picornavirus (RNA virus).
 Three immunological distinct strains have been
isolated
1. Type-1-Brunhilde,
2. Type-2-Lanchi,
3. Type-3-Leon.
 Immunity to one does not result in immunity to the
other two.

16. Mode of Transmission
 Spread by faecal/oral route.
 Inhalation or entry through conjunctiva of droplets
of respiratory secretions may also be possible
modes of entry in close contacts of patients in
early stage of disease.
 Once ingested the virus multiplies in the
nasopharynx and gastrointestinal tract.
 Penetration of GI tract results in viraemia but
CNS involvement occurs in only a very small
proportion.
 Most infected patients are asymptomatic.
 Virus excretion continues in the faeces for as long
as three months after the initial infection – carrier
state

17. MODE OF TRANSMISSION

18. Pathogenesis

19. Pathophysiology of polio infection in
nervous system
 Only 5% of infected patients have selective nervous system
involvement after viremia.
 The poliovirus enters the nervous system by either crossing the
blood-brain barrier or by axonal transportation from a peripheral
nerve.
 It can cause nervous system infection by involving the precentral
gyrus, thalamus, hypothalamus, motor nuclei of the brainstem
and surrounding reticular formation, vestibular and cerebellar
nuclei, and neurons of the anterior and intermediate columns of
the spinal cord.
 The nerve cells undergo central chromatolysis along with an
inflammatory reaction while multiplication of the virus precedes
onset of paralysis.
 As the chromatolysis process goes on further, muscle paralysis
or even atrophy appears when fewer than 10% of neurons
survive in the corresponding cord segments.
 Gliosis develops when the inflammatory infiltrate has subsided,
but most surviving neurons show full recovery.

20. Pathogenesis

21. Pathogenesis

22. Clinical presentation
 Prodromal stage or pre paralytic stage
 Paralytic stage – can further divided into
 Acute stage
 Convalescent stage
 Stage of recovery
 Residual stage or post polio syndrome

23. Preparalyitc stage
 Few hours to a few days and 1 to 3 days is the
usual duration.
 Fever, malaise, sweating, Headache, Sore throat,
Slight Cough and Diarrhea or constipation.
 It may improve or progress to severe symptoms
like
• Backache
• Joint pains.
• Pyrexia of variable duration and severity.
• Mild neck stiffness.
• Irritability.

25. Acute stage
 3 to 6 weeks from the onset of Poliomyelitis.
 Muscle tenderness is the most important
sign seen in this stage esp in calf muscles

26. Convalescent stage
 Duration 3 months.
 Spinal Type:
 Asymmetric paralysis. Paralysis develops;
widespread or localised; ascending or descending,
maximal 24 hours after onset of this stage.
 The lower limb muscles are more often involved.
 Muscles fasciculate.
 Muscle pain worsens
 May involve respiratory muscles.
 Flexion contractures of hip, knee and equinus
deformity of the ankle are common.

27.  Bulbar Type:
 Involvement muscles innervated by crainal nerve -
Pharyngeal, laryngeal, lingual and facial weakness
 The early signs of respiratory involvement
includes breathing difficulty, feeling of suffocation,
slight cyanosis, use of sternomastoids, alae nasae
and other accessory muscles of respiration.
 Spinobulbar: This type has a combination of both
spinal and bulbar type.
 Postencephalic: Mental disturbance, coma, paralysis
of facial muscles, symptoms similar to meningitis like
headache, vomiting, neck stiffness may occur

29. Recovery stage
 This stage extends for almost 2 years.
 Thus muscle in the polio patient can be
strengthened to their maximum capacity upto 2
years.

31. Residual stage or Post Polio
Syndrome
 Post-polio syndrome (PPS) is a condition that
affects polio survivors years after recovery from
an initial acute attack of the poliomyelitis virus.
 Halstead introduced the term "post-polio
syndrome" in 1986, and he published revised
criteria for diagnosing PPS in 1991, in which new
muscle weakness was introduced
 Other terms - "late effects of polio" (LEoP) and
"postpolio muscular atrophy."

32. Criteria for the diagnosis of PPS
were published by March of Dimes
 Prior paralytic poliomyelitis with evidence of motor neuron loss,
as confirmed by history of the acute paralytic illness, signs of
residual weakness and atrophy of muscles on neurologic
examination, and signs of denervation electromyography (EMG)
 A period of partial or complete functional recovery after acute
paralytic poliomyelitis, followed by an interval (usually 15 y or
more) of stable neurologic function
 Gradual or sudden onset of progressive and persistent new
muscle weakness or abnormal muscle fatigability (decreased
endurance), with or without generalized fatigue, muscle atrophy,
or muscle or joint pain; sudden onset may follow a period of
inactivity, or trauma or surgery; less commonly, symptoms
attributed to PPS include new problems with breathing or
swallowing.
 Symptoms persist for at least a year
 Exclusion of other neurologic, medical, and orthopedic problems

33. Pathophysiology of PPS
 Pathology in post polio syndrome is not well understood but
several hypothesis had been formulated.
 Disintegration of overused motor units:
 Decompensation of a chronic denervation and reinnervation
process to the extent that the remaining healthy motor neurons
can no longer maintain new sprouts; thus, denervation exceeds
reinnervation.
 Reactivation of polio virus: Motor neuronal loss due to
reactivation of a persistent latent virus.
 Immune system dysfunction:
 Foci of perivascular and interstitial inflammatory cells have been
found on 50% of biopsies of patients with PPS. Activated T cells
and immunoglobulin M and immunoglobulin G antibodies specific
for gangliosides also have been found.
 The loss of strength due to the usual stresses of aging and
weight gain can produce PPS .
 Infection of the polio survivor's motor neurons by an

34. Signs and Symptoms of PPS
 Progressive muscle and joint weakness and pain
 General fatigue and exhaustion with minimal
activity
 Muscle atrophy
 Breathing or swallowing problems
 Sleep-related breathing disorders, such as sleep
apnea
 Decreased tolerance of cold temperatures
 Flat-back syndrome

36. Investigations
 CSF Examination: Mildly elevated protein content in CSF from
40 to 50 mg/100 ml
 Throat washing: Throat washing is taken and assessed for the
virus. The washings are incubated at a favourable atmosphere in
a culture media.
 Stool samples are also examined for polio virus
 Blood tests: Blood is tested for antibodies for polio virus.
 Fingerprinting the polio virus
 Once the polio virus is isolated it is tested by a special test called
oligonucleotide mapping (fingerprinting) or genomic sequencing.
This is essentially looking at the genetic sequence of the virus to
detect if the origin of the virus is “wild type” or “vaccine like”.
 Wild type virus naturally occurs in the environment and may
occur as 3 subtypes – P1, P2 and P3. Vaccine like virus is
derived after a spontaneous mutation of the genes of the virus in
the polio vaccine.

37. Investigations
 Plain radiograph and CT
 With acute infection, no radiographic features are
typically evident.
 Chronically, findings are characterized by atrophy of
involved areas, including of bone and muscle, which
may be similar to other neuromuscular disorders.
 MRI
 Neuroimaging may reveal ALS-like abnormalities in
the affected areas of the ventral motor tracts in the
spine and/or motor cortex, which are characteristically
hyperintense.
 Extensive fatty muscle atrophy may be seen in
affected areas of the musculoskeletal system, which
may be unilateral or bilateral.

38. Treatment
 No treatment, Supportive measures
 Prevention - Vaccination: Salk and Sabin vaccination
 Acute stage:
 Rest-The child should not be over handled.
 Isolation
 Booster dose
 Nutrition-Diet rich in" Protein".
 Sister Kenny's Bath: This is a form of moist heat. This
helps to resolve inflammation to some extent.
 Massage should not be given as it may cause more
damage due to which the patient may not be able to
walk later on

39.  Convalescent stage Treatment
 Muscle Charting.
 Positioning.
 Changing the position-Turning the patient every 2
to 4 hours and night prevents bed sores and
keeps the skin dry
 Residual stage treatment
 Patient is given combination of stretching,
strengthening and calliperization.
 Tailor-made calipers and splints can prevent the
deformity from aggravating. Eg., knee calipers,
below knee brace, AFO, KAFO etc.,

40. Orthopaedic operations in patients
with residual poliomyelitis
 The subcutaneous method of division:
Hip and knee contractures of over 30 degree – (factor
responsible for the deformity in young child is a tight
tensor fascia lata and ilio-tibial band. In the older child
or adult, other ligamentous and tendinous structures
play an important part and must be divided as well)
 Tendon transfer to re-establish muscle power
 Muscle transplantation to replace a paralysed muscle
 Stabilization of relaxed or flail joint
 Arthrodesis
 Limb lengthening
 Joint replacement surgery
 Ilizarov techniques

41. Rehabilitation
 Physical therapy
 Occupational therapy
 Speech therapy
 Vocational therapy

42. THANK YOU