Poliomyelitis
Definition:
It is an acute viral infection of human, which tends to localize in
the motor neurons of the central nervous system specially the spinal cord
and brain stem, causing a lower motor neuron type of paralysis without
sensory loss. The infant gets sub-clinical infection; the older child gets
paralysis while the adult often dies because of the extensive paralysis.
Virology:
Three types of polioviruses are known since 1951:
- Type 1: Brunhilde: It is the commonest poliovirus in Egypt.
- Type 2: Lansing.
- Type 3: Leon.
The child may be attacked by the three types of polioviruses
successively, as infection by one virus does not immune the child against
the other two types. The virus can be isolated from the pharyngeal
secretions one week before and two weeks after the onset of clinical
infection. It can be found in the stool for a month or longer after the
infection started.
History:
- It has been first occurred in the time of the ancient Egyptians.
- In 1789, Underwood was the first to describe poliomyelitis.
- In 1834, the first epidemic of poliomyelitis occurred.
- In 1855, Duchenne descried the pathology process in poliomyelitis.
- In 1908, Landstener transmitted poliomyelitis to a monkey.
- In 1951, the three known polioviruses were isolated and identified.
- In 1958, Sabine vaccine was used for the first time.
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Pathology:
1. Acute stage
Poliomyelitis is a generalized infection which may involve the
whole body. Motor involvement of the spinal cord and brain stem is the
only permanent manifestation:
a) Following multiplication in the pharynx and intestine, the virus
penetrates the intestinal wall and travels in blood to all body parts. So,
viral multiplication plays a major role in the neural damage.
b) In 1% to 5% of the affected persons, the virus invades the spinal cord,
where it has a predilection for motor neuron in the anterior horn cells
(AHC), causing a variable degree of paralysis. Then, cells either die or
shed the virus and regain a normal morphologic appearance.
c) Areas in which lesion may occur include:
- Spinal cord, especially the anterior horn cells; though to a lesser extent
the intermediate and dorsal horns.
- Medulla, including the cardio-respiratory centers.
- Cerebellum, midbrain, thalamus and hypothalamus.
- Motor cortex.
d) The pathological changes consist mainly of:
- Hyperemia and edema of the piamater (the innermost of the meninges).
- Minute capillary hemorrhage.
- Perivascular infiltration of lymphocytes (a variety of white blood cells),
which block off the small blood vessels.
- Pressure exerted on anterior horn cells and interstitial tissue is most
striking in the lumber and cervical enlargement of the cord.
e) The anterior horn cells show:
- Dissolution of mitochondria.
- Progressive chromatolysis.
- Shrinkage of nuclei.
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- Degeneration of cell bodies, which extends to the axons.
- Disappearance of the AHC, to be replaced by sclerotic tissues.
- Complete degeneration of the interstitial cells.
f) As the virus invades the central nervous system, the extent of
neurological and functional recovery is determined by the number of
motor neurons which:
- Recover and resume their normal function.
- Re-survive unimpaired.
- Develop terminal axonal sprouts to re-innervate muscle fibers.
2. Chronic stage
A. Locomotor system:
1. Muscles:
a) Destruction of the AHC causes a variable degree of paralysis, ranging
from minimal degree which may recover completely, to severe degree.
b) The lower limbs are usually more involved than the upper limbs.
Certain muscle groups tend to be more often involved than other groups.
These groups include: Hip and knee extensors, ankle dorsiflexors,
intercostal muscles, spinal muscles, thenar muscles, deltoid and triceps.
c) The paralyzed muscles show: Atrophy, fatty infiltration and
replacement by connective tissue. Contractures may occur due to partial
or complete fibrosis of the paralyzed muscles. Secondary contractures of
ligaments and joint capsules may result from long-standing shortening of
muscles and tendons.
2. Bones and joints:
- The lack of muscle pull in addition to vascular and neurological causes
resulting from the effect of paralysis, lead to shortening in the length and
diameter of bones in the growing limb. Fractures may also occur.
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- The effect of long-standing contractures on the joint surfaces may cause
them to become deformed and subluxated or dislocated.
- Unsupported walking on weak joints may also lead to some changes.
- Intra-articular adhesions may form if attempts are made to straighten the
joints by vigorous manipulations.
B. Skin and subcutaneous tissues:
Paralyzed limbs may become edematous in cold climates due to
hemostasis (stagnation of blood in its vessels) and gravity.
C. Respiratory system:
Lung infections are common due to paralysis of the respiratory
muscles (diaphragm and intercostal muscles).
D. Bulbar (medulla) palsy:
Bulbar paralysis usually recovers with no residual effects. Bulbar
palsy in the acute stage may result in lung abscess in the chronic stage
due to the inhaled secretions.
Causes of deformities:
1. Muscle spasm:
The initial cause of deformities in polio appears to be muscle
spasm, followed by interstitial fibrosis and collagen deposition in paretic
muscle groups. The exact cause of muscle spasm is unknown but it
appears to be due to in-coordinated involuntary contractions of the
surviving fibers in the partially paralyzed muscles.
2. Effect of gravity:
Gravity may lead to equinus of the ankle and adduction of the
shoulder.
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3. Effect of posture:
Prolonged bed rest, particularly in severely paralyzed patients
without adequate physical therapy may cause flexion deformity of the
hip, knee and ankle joints. This is the commonest deformity in
poliomyelitis patients after muscle imbalance.
4. Short leg and other associated deformities:
A short leg or a flexed hip may cause the pelvis to tilt and a
compensatory scoliosis in the spine. If this deformity is left uncorrected,
it may become permanent.
5. Weight bearing on weak joints:
This may lead to genu recurvatum or valgus ankle. The deformity
becomes worse with stretching of the ligaments or the joints without
external support to the deformed joint.
6. Progress of contractures:
All the mentioned deformities may progress if left uncorrected in
children where bone growth is not equalized. Untreated mild spinal
deformity may lead to severe and permanent scoliosis or kyphosis.
Common deformities:
a) Hip joint: Flexion, abduction and external rotation is the commonest
deformity due to relative weakness of the opposing muscle groups.
b) Knee joint: The commonest knee deformities are flexion deformity
due to paralysis of the knee extensors and mild valgus deformity (30%).
Genu recurvatum may occur due to early weight bearing on a week knee.
Lateral rotation of the tibia on the femur and lateral subluxation of the
knee may also occur.
c) Ankle joint: Equinus deformity due to weak dorsiflexors is a common
deformity. Valgus, varus and cavus foot are other commonly occurring
deformities.
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Causes of muscle weakness in poliomyelitis:
 Direct causes (viral infection):
1. Permanent destruction of the motor cells with subsequent atrophy and
paralysis of the denervated muscle fibers.
2. Temporary and reversible impairment of nerve cell function due to an
inflammation or pressure.
 Indirect causes:
1. Early:
- Reflex inhibition of muscular activity due to pain.
- Impaired muscle cellular function from nutritional and metabolic
disturbance.
2. Late:
- Insufficient exercise as a result of immobilization.
- Excessive activity or over-stretching of a weakened muscle.
- Persistent limitation of motion due to contractures and shortening.
- Habitual positioning and muscular imbalance.
- Persistent reflex inhibition of muscular activity, as a result of prolonged
and sustained activity of antagonistic musculature.
Vaccination:
There are two types of polio vaccines:
a) Salk vaccine:
It is composed of killed viruses, given by injection. It has the
advantage of being safe and not being suppressed by the intestinal
entroviruses. Salk vaccine has the disadvantage of:
* The need for repeated injections.
* Delayed immunity as it needs about three weeks to achieve.
* Incomplete immunity.
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b) Sabine vaccine (trivalent vaccine):
It is composed of attenuated live polioviruses. It has the
advantages of having faster immunity within about three days and longer
immunity, which may be long-life. It has the disadvantage of being
prevented from action by the intestinal entroviruses. Three drops of the
Sabine vaccine are to be administered into the back of the mouth or on a
lump of sugar. Dosage should start at the age of two or three months, to
be repeated three successive times at 4-6 weeks interval. A booster dose
at the age of 18 months and another dose at school entry are also
required.
Clinical features:
Initial incubation period, which varies from seven to twenty one
days, is the common interval between infection and the clinical illness.
After the incubation period, four responses may occur:
1. Asymptomatic polio: This can only be diagnosed during an epidemic or
if the virus is cultured from the stool.
2. Abortive polio: There is a flu-like illness with fever, nausea, vomiting,
sore throat, headache and constipation. The virus may also be cultured
from the stool.
3. Non-paralytic polio: Three or four days after the above initial
symptoms, the patient may develop a stiff neck. Moreover, deep and
superficial reflexes are usually depressed. Temporary urinary retention
and constipation without sensory loss may follow.
4. Paralytic polio: The signs and symptoms in paralytic polio are very
variable in both duration and severity. After few days from paralytic
polio, the lower motor neuron paralysis develops. The distribution of
paralysis is asymmetric and patchy. According to the affected area, three
forms are found:
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a) Spinal form: It may affect any group of muscles from the neck, trunk
or limbs including the diaphragm. In addition, there may be transient
involvement of the bladder with the subsequent urinary retention.
b) Bulbar paralysis: The motor nuclei of the cranial nerves may be
affected with or without involvement of the vital centers. The most
important sign of bulbar paralysis is the inability to swallow (dysphagia)
due to pharyngeal paralysis. In addition, the patient cannot cough
properly due to paralysis of the larynx.
c) Encephalitic form: There will be some degree of motor paralysis in
addition to drowsiness, disorientation, mental disturbance and even
comma may occur.
Treatment:
1. Acute stage
Paralytic stage of poliomyelitis is always preceded by the
prodromal or pre-paralytic stage. Treatment during this stage includes:
- Obligatory rest in bed.
- Maintain fluid and electrolyte balance.
- Exhausting examinations are contraindicated.
- Comfortable and relaxed position should be carried out.
- Minimize muscular pains during handling.
- Avoid injection and non-emergency operations.
- Care of skin to avoid bedsores.
- Daily breathing exercises to avoid respiratory infection.
At the immediate post-acute stage, concentration should be directed to:
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Encourage periods of near-normal body alignment within limits of pain.
- Use moist heat when the patient is afebrile to relieve muscle spasm.
- Forty-eight hours after the patient is afebrile, range of motion and
gentle stretching exercises should be applied daily.
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- Maintain correct posture and avoid any possible deformity using
pillows, footboards and splints.
- As tightness and resistance to movement subside and muscle balance is
gained, progressive sitting and weight-bearing exercises are required.
2. Convalescent stage
As there is decreased capacity for work, energy expenditure should
be decreased to the lowest possible level to prevent over-exhaustion.
a) Range of motion exercises:
They aim to prevent contractures. This can be achieved by:
- Passive movement within the limits of pain.
- Muscle stretching but avoid overstretching.
- Utilization of splints and bracing to prevent deformities, assist function
and avoid undesirable substituted actions.
b) Mobilization:
The patient should be out of bed early unless paralysis is very
severe. He / she should be exercised first in bed then in chair before
being stood up. Walking aids can be used in this stage.
c) Muscle reeducation:
- Improve muscle strength of all muscles in the body.
- Facilitation of weak and paralyzed muscles either by manual,
mechanical or electrical methods such as “quick stretching, tapping,
proprioceptive neuromuscular stimulation (PNF), ice application,
faradic stimulation and vibration techniques”.
- Concentration should be directed to obtain maximum strength of
appropriate muscle groups to compensate the action of weak muscles,
prevent substituted action and prevent deformity.
- Avoid excessive exercises to prevent muscle exhaustion, fatigue,
undesired movement and energy loss.
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d) Improvement of respiration: If respiratory paralysis occurs, the role of
physical therapy is essential to keep the lungs free. If the patient cannot
cough properly, breathing exercises and postural drainage may be used.
3. Chronic stage
a) Improve functional activity:
- Overdevelop residual abilities to substitute for lost motions.
- Increase proprioceptive awareness through repetitive practice.
- Improve strength of the remaining muscles by high resistive exercises.
- The use of supportive devices is indicated.
- Surgical procedures are utilized to regain motion and correct deformity.
b) Management of limb shortening:
- Treatment of leg shortening should be conservative in most cases.
- Shortening of one cm requires no treatment, while more shortening
requires compensation through the use of medical shoes or braces.
c) Electrical stimulation:
As poliomyelitis disappeared altogether from Europe and most of
the well-developed and advanced industrialized countries, there is no
international literature concerning management of poliomyelitis since
1960s. Unfortunately, as such infectious disease still exists in a large
proportion of many poor countries; discussion of the new methods for
treatment of poliomyelitis is undoubtedly fruitful.
Galvanic current (a long-width stimulus, more than 100 msec) is
able to stimulate denervated muscle fibers, having resting membrane
potential of (-90 mv), which is higher than that of the nerve (-70 mv). As
poliovirus affects motor neurons unselectively, a single muscle may have
some affected and some spared muscle fibers. So, galvanic current will
then stimulate both the denervated and innervated muscle fibers.
Excessive stimulation of innervated muscle fibers leads to their fibrosis.
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On the other hand, the use of faradic stimulation (a short-width
stimulus, less than 100-msec width) will enhance activation of the
recovering fibers whose nerve cells were compressed. Faradic
stimulation can also help in improving the muscle’s general condition
and accelerating development of functional abilities in both convalescent
and chronic stages of poliomyelitis.
d) Vibration:
The use of vibration in the treatment of poliomyelitis has not been
tried before because poliomyelitis as a disease disappeared completely
from many countries, in which scientific researches concerning
neurophysiology are well advanced. Among aims of physical therapy
applications are to activate partially affected muscles and to give the
patient the feeling of movement and posture. It is also important to
increase afferent impulses to the motor neurons by increasing the area
and receptors stimulated.
According to the neurophysiologic mechanism of vibration,
vibrator is an excellent tool for increasing the amount of afferent
impulses toward motor neuron pool as it is the most effective stimulus to
Ia nerve fibers, which has a direct contact with motor neuron pool.
During application of vibration, the patient should be relaxed and muscle
fibers to be vibrated are fairly stretched.
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