Poliomyelitis

• Polio – Gray matter

• Myelitis – Inflammation of spinal cord
• First described by Michael Underwood in 1789
• 1855, Duchenne descried the pathology
process in poliomyelitis
 Introduction
• Acute poliomyelitis is a viral infection localized
in the anterior horn cells of the spinal cord
and certain brainstem motor nuclei.

Type 1: Brunhilde
Type 2: Lansing
Type 3: Leon
 Introduction

• One of three types of poliomyelitis viruses

usually is the cause of infection, but other
members of the enteroviral group can cause a
condition clinically and pathologically
indistinguishable from poliomyelitis.
• Initial invasion by the virus occurs through the
gastrointestinal and respiratory tracts and
spreads to the central nervous system through
a hematogenous route.
 Introduction

• Affects children younger than 5 years old in

developing tropical and subtropical countries
and unimmunized individuals in other
temperate climates
• Administration of at least two and preferably
three doses of the Sabin oral polio
vaccine(OPV), containing all three types of
attenuated virus, can prevent the disease.
 Pathology
• Poliomyelitis virus invades the body through the
oropharyngeal route, it multiplies in the alimentary tract
lymph nodes and spreads through the blood, acutely
attacking the anterior horn ganglion cells of the spinal
cord, especially in the lumbar and cervical
enlargements.
• The incubation period is 6 to 20 days.
• The anterior horn motor cells may be damaged directly
by viral multiplication or toxic by-products of the virus
or indirectly by ischemia, edema, and hemorrhage in
the glial tissues surrounding them.
 Distribution Of Polio Paralysis

• Lower limb 92 %
• Trunk + LL 4%
• LL + UL 1.33 %
• Bilateral UL 0.67 %
• Trunk + UL + LL 2%
• The number of individual muscles affected by the
resultant flaccid paralysis and the severity of paralysis
vary; the clinical weakness is proportional to the number
of lost motor units.
• Weakness is clinically detectable only when more than
60% of the nerve cells supplying the muscle have been
destroyed.
• Muscles innervated by the cervical and lumbar
spinal segments are most often affected, and
paralysis occurs twice as often in the lower
extremity muscles as in upper extremity muscles.
• In the lower extremity, the most commonly
affected muscles are the quadriceps, glutei,
anterior tibial, medial hamstrings, and hip flexors;
• In the upper extremity, the deltoid, triceps, and
pectoralis major are most often affected.
 Progression

• The potential for recovery of muscle function

depends on the recovery of damaged, but
not destroyed, anterior horn cells.
• Most clinical recovery occurs during the first
month after the acute illness and is almost
complete within 6 months, although limited
recovery may occur for about 2 years
• A muscle paralyzed at 6 months remains
paralyzed
 Clinical course
• The course of poliomyelitis can be divided into three
stages: acute, convalescent, and chronic.
• Post polio syndrome.
 Acute stage

• The acute stage generally lasts 7 to 10 days.

Symptoms range from mild malaise to
generalized encephalomyelitis with
widespread paralysis.
• Differential diagnoses include Guillain-Barré
syndrome and other forms of
encephalomyelitis.
 Acute stage

• Treatment of poliomyelitis in the acute stage

generally consists of bed rest, analgesics, hot
packs, and anatomical positioning of the limbs
to prevent flexion posturing and contractures.
• Padded foot boards, pillows, sandbags, and
slings can help maintain position. Gentle,
passive range-of-motion exercises of all joints
should be carried out several times each day
 Convalescent stage
• The convalescent stage begins 2 days after the
temperature returns to normal and continues for 2
years.
• Muscle power improves spontaneously during this
stage, especially during the first 4 months and more
gradually thereafter. Muscle strength should be assessed
monthly for 6 months and then every 3 months.
 Convalescent stage
• Physical therapy should emphasize muscle activity in
normal patterns and development of maximal capability
of individual muscles. Muscles with more than 80%
return of strength recover spontaneously without
specific therapy. An individual muscle with less than
30% of normal strength at 3 months should be
considered permanently paralyzed.
• Vigorous passive stretching exercises and wedging casts
can be used for mild or moderate contractures. Surgical
release of tight fascia and muscle aponeuroses and
lengthening of tendons may be necessary for
contractures persisting longer than 6 months. Orthoses
should be used until no further recovery is anticipated.
 Chronic stage
• The chronic stage of poliomyelitis usually begins 24
months after the acute illness.
• During this time, the orthopaedist attempts to help
the patient achieve maximal functional activity by
management of the long-term consequences of
muscle imbalance.
 Chronic stage

• Goals of treatment include correcting any

significant muscle imbalances and preventing
or correcting soft-tissue or bony deformities.
• Static joint instability usually can be
controlled indefinitely by orthoses.
• Dynamic joint instability eventually results in
a fixed deformity that cannot be controlled
with orthoses
Post Polio Syndrome
 Criteria
• Prior paralytic poliomyelitis with evidence of
motor neuron loss
• A period of partial or complete functional
recovery after acute paralytic poliomyelitis
• Slowly progressive and persistent new muscle
weakness or decreased endurance
• Symptoms that persist for at least a year
• Exclusion of other neuromuscular, medical,
and skeletal abnormalities
 Deformity

• Usually affected muscles/groups include: Hip

and knee extensors, ankle dorsiflexors,
intercostal muscles, spinal muscles, thenar
muscles, deltoid and triceps.
 Foot
• claw toes
• cavovarus foot
• dorsal bunion
• talipes equinus
• talipes equinovarus
• talipes cavovarus
• talipes equinovalgus
• talipes calcaneus.
 Knee

• flexion contracture of the knee

• quadriceps paralysis
• genu recurvatum
• flail knee
 Hip
Paralysis of the muscles around the hip can cause
severe impairment.
• flexion and abduction contractures of the hip
• hip instability and limping caused by paralysis of
the gluteus maximus and medius muscles
• paralytic hip dislocation
 Abdomen, Back, Scapula, and Neck
Weakness or paralysis of the rectus abdominis produces an anterior tilt of the pelvis
and an increase in lumbar lordosis, both of which are exaggerated if the hip
flexors are active.
Unilateral weakness of the quadratus lumborum produces a lateral deviation of the
spine or a pelvic obliquity with secondary compensatory changes proximally.
Unilateral weakness of the latissimus dorsi can produce a similar effect.
When the serratus anterior and pectoralis major are active, the rhomboids are
weak, and the shoulder is drooping, the weight of the shoulder girdle is thrown
anterior to the angle of the ribs and together with the pull of the active muscles
tends to flatten the ribs.
Contractures of unopposed muscles that pull diagonally or laterally, such as the
transversalis, serratus anterior, and abdominal obliques, together with an
unbalanced pull of the pectoralis major, latissimus dorsi, and quadratus
lumborum, contribute to rotary and lateral deformities of the spine and ribs.
Paralysis of various muscles around the shoulder also can contribute to paralytic
scoliosis in the cervical and upper thoracic spine, drooping and instability of the
shoulder girdle, and deformity of the chest.
 Shoulder

• Paralysis of deltoid
• Paralysis of Subscapularis, Suprascapularis,
Supraspinatus, or Infraspinatus
• Flail shoulder
 Elbow and forearm

• Flexion contracture of elbow

• Pronation Contracture
 Surgical options

1. To get the patient walking;

2. If the patient is a child, correct factors that
will create deformity with growth;
3. To correct factors that will obviate or reduce a
lifetime dependency on an external brace;
4. To correct upper extremity problems;
5. To treat scoliosis.
 Tendon transfer

• To provide active motor power to replace

function of a paralyzed muscle or muscles
• To eliminate the deforming effect of a muscle
when its antagonist is paralyzed
• To improve stability by improving muscle
balance.
Tendon transfer shifts a tendinous insertion from its normal attachment
to another location so that its muscle can be substituted for a paralyzed
muscle in the same region
• The muscle to be transferred must be strong enough to accomplish
what the paralyzed muscle did or to supplement the power of a
partially paralyzed muscle
• freed end of the transferred tendon should be attached as close to
the insertion of the paralyzed tendon
• transferred tendon should be retained in its own sheath or should be
inserted into the sheath of another tendon
• nerve and blood supply to the transferred muscle must not be
impaired or traumatized
• Joint should be supple
• transferred tendon must be securely attached to bone under tension
slightly greater than normal
• Agonists are preferable to antagonists
• range of excursion similar to the one it is reinforcing or replacing
 Bony procedures

• Osteotomy and arthrodesis

• Knee
– Distal femur osteotomy
– Arthrodesis
• Foot and ankle
– Calcaneal osteotomy
– Subtalar arthrodesis
– Triple arthrodesis
Thank you