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: BrunhildeType 2: LansingType 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-Barrésyndrome 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. Orthosesshould 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, thenarmuscles, 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 NeckWeakness 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

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