Sma Et Polio

8/12/2019 Sma Et Polio

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ST. PAUL UNIVERSITY ILOILO

College of Physical Therapy

2014

Seminar 2

SPINAL MUSCULAR ATROPHY and POLIOMYELITIS

Group # 2

Section A:

Leaders: Dariza Badeo & Mitchell Teodosio

Members: Trisha Jane Wong

Jahanne Rafio

John Xand Acuros

Rustom John Ordaniel

Ervin Sales

Eduardo Montinola

Section B:

Leaders: Floyd Juatas & Justine Vee Guardapavo

Members: Jethro Von Guardapavo

Cirille JuarezKent Lauro Almodin

Stella Tingson

BSPT IV

January 6, 2014


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Table of Contents

Definition of Terms -------------------- 3

Anatomy et Physiology -------------------- 4-5

SPINAL MUSCULAR ATROPHY

Definition of Condition -------------------- 6

Etiology -------------------- 6

Epidemiology -------------------- 6-7

Classification -------------------- 7-8

Pathomechanism -------------------- 8

Signs and Symptoms -------------------- 8

Differential Diagnosis -------------------- 8-9

Diagnostic Tools -------------------- 9-10

Medical Management -------------------- 10

Surgical Management -------------------- 10-11

PT Management -------------------- 11

Prognosis -------------------- 12

POLIOMYELITIS

Definition of Condition -------------------- 13

Etiology -------------------- 13

Epidemiology -------------------- 13

Classification -------------------- 14-15

Pathomechanism -------------------- 16

Signs and Symptoms -------------------- 16

Differential Diagnosis -------------------- 17

Diagnostic Tools -------------------- 17-18

Medical Management -------------------- 18

Surgical Management -------------------- 18-19

PT Management -------------------- 19

Prognosis -------------------- 20

References -------------------- 21


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I. Definition of terms

Apoptosis programmed cell death

Bulbar motor nuclei involvement or Bulbar palsy refers to impairment of functionof the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron

lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of

the lower cranial nerves outside the brainstem. It is characterized by dysarthria.

ConusMedullaris - is the tapered, lower end of the spinal cord.

Encephalomeningitis is a fatal medical condition that is characterised by an

inflammation of the meninges of the brain and spinal cord. It may be caused by apathogenic infection by a disease vector that can penetrate the barriers of the

Central Nervous System.

FilumTerminale - the slender threadlike prolongation of the spinal cord below the

origin of the lumbar nerves : the last portion of the pia mater.

Hypotonia - is a medical term that describes decreased muscle tone.

Motor unit -The muscle fibers innervated by a single anterior horn cell.

Myasthenia gravis is an autoimmune neuromuscular disease leading to fluctuating

muscle weakness and fatigue.

Spinal Cord - is a long, thin, tubular bundle of nervous tissue and support cells that

extends from the brain

Somatotopically - point-for-point correspondence of an area of the body to aspecific point on the central nervous system.

Viraemia is a medical condition where viruses enter the bloodstream and hence

have access to the rest of the body.


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II. ANATOMY AND PHYSIOLOGY

Spinal Cord

- Approximately 42-45 cm in length

- Spinal Column approx 72 cm in length.

- Begins at the Foramen Magnum

- Terminates at L1-L2, L2-L3

- Tapers off into CONUS MEDULLARIS and forms an apex called FILIUM TERMINALE

- Attached are 31 spinal nerves

A. Anterior Gray Matter

a. MEDIAL

-present in most segments

-for the innervation of skeletal muscles, trunk, intercostal and abdominal muscles

b. LATERAL

-present in CERVICAL and LUMBOSACRAL seg.

-for the innervation of skeletal muscles.

c. CENTRAL

-smallest

-present in CERVICAL and LUMBOSACRAL seg

B. Posterior Gray Matter

a. Substantia Gelatinosa

-found along the ENTIRE length of the cord-for Pain, Touch and Temperature

b. Nucleus Propius

-found along the ENTIRE length of the cord

-for 2 point discrimination

c. Clarke's Column-found on C8-L4

-for proprioception

d. Visceral Afferent Nucleus


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-found on T1-L3

-for Visceral Sensation

C. Lateral Gray Matter

a. Preganglionic Sympathetic Fibers

-found on T1 to L3

b. Preganglionic Parasympathetic Fibers

-found on S2-S4

Motor neurons

- Also called efferent nerves and effector neurons, that carry signals from the spinal cordto the muscles to produce movement.

Anterior horn cell

- also called the anterior cornu, anterior column or ventral horn is the ventral (front) greymatter section of the spinal cord.

- It is one of the three grey columns and it contains motor neurons that affect the axialmuscles while the posterior horn receives information regarding touch and sensation.

- It is where the cell bodies of alpha motor neurons are located.

SMN1 gene

- provides instructions for making the survival motor neuron (SMN) protein.

SMN protein

- is a 294 amino acid polypeptide that is expressed in all cell types of vertebrateorganisms which is necessary for the survival of motor neurons.

- it is localized in the cytoplasm and play a crucial role in the assembly of spliceosomaluridine-rich small nuclear ribonucleoprotein (U snRNP) complexes.

SnRNPs

- are made up of small nuclear RNA (snRNA) and a group of seven proteins that areknown as Sm ribonucleoproteins. These seven proteins are what make the core of snRNPextremely stable.

- are essential to the job of splicing introns in pre-mRNA during the post-transcriptionalmodification of RNA that occurs after transcription.

In cells, the SMN protein plays an important role in processing molecules called messengerRNA (mRNA), which serve as genetic blueprints for making proteins. Messenger RNA beginsas a rough draft (pre-mRNA) and goes through several processing steps to become a final,mature form. The SMN protein helps to assemble the cellular machinery needed to processpre-mRNA.


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SPINAL MUSCULAR ATROPHY

III. Definition of Condition

Spinal muscular atrophy (SMA) is an autosomal recessive disease caused by a

genetic defect in the SMN1 gene, which encodes SMN (Survival Motor Neuron) a protein

widely expressed in all eukaryotic cells. SMN1 is apparently selectively necessary for

survival of motor neurons, as diminished abundance of the protein results in death of

neuronal cells in the anterior horn of the spinal cord and subsequent system-wide muscle

wasting.

IV. Etiology:

SMA is caused by a missing or abnormal (mutated) gene known as survival motor

neuron gene 1 (SMN1). In a healthy person, this gene produces a protein in the body called

survival motor neuron (SMN) protein. In a person with mutated genes, this protein is absent

or significantly decreased, and causes severe problems for motor neurons. Motor neurons

are nerve cells in the spinal cord which send out nerve fibers to muscles throughout the

body. Since SMN protein is critical to the survival and health of motor neurons, nerve cellsmay shrink and eventually die without this protein, resulting in muscle weakness. As a child

with SMA grows, it is difficult for his/her weakened muscles to keep up with the demands of

daily activities. The resulting weakness can also lead to bone and spine changes that may

cause breathing problems and further loss of function.

V. Epidemiology:

Frequency

U.S., SMA are the 2nd most common autosomal-recessive inherited disorder after cystic

fibrosis.

SMA type 1 affects approximately 1 per 10,000 live births.

SMA type 2&3 affects approximately 1 per 24,000 births.

SMA type 1&3 each account for about of cases, whereas,

SMA type 2 is the largest group and accounts for of all cases.


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Mortality/Morbidity

The mortality rates of SMA are inversely correlated with the age at onset. High death rates

are associated with early onset disease. In patients with SMA type 1, the median survival

is 7 months, with a mortality rate of 95% by age 18 months.

Respiratory infections account for most deaths.

In type 2 SMA, the age of death varies, but death is most often due to respiratory

complications.

Age - According to the ISMAC system, the age of onset for SMA is as follows:

SMA type 1 : onset is from birth to 6 months

SMA type 2 : onset is between 6 and 18 months

SMA type 3 : onset is after 18 months

SMA type 4 : onset in adulthood (mean onset, mid 30s).

VI. CLASSIFICATION

SMA Type I( Acute infantile or Werdnig-Hoffman disease)

They have severe, progressive mm weakness and flaccid or reduced muscle tone

(hypotonia). Bulbar dysfunction includes poor suck ability, reduced swallowing, and

respiratory failure. Patients have no involvement of the extraocular muscles, and

facial weakness is often minimal or absent. They have no evidence of cerebral

involvement, and infants appear alert.

SMA Type II ( Chronic infantile form )

The most common form of SMA, and some experts believe that SMA Type II may

overlap types I and III. Patients may have developmental motor delay. Infants with

SMA type II often have difficulties with sitting independently or failure to stand by 1

year of age. An unusual feature of the disease is a postural tremor affecting the

fingers. This is thought to be related to fasciculation in the skeletal muscles.

SMA Type III (Chronic juvenile or Kugelberg-Welander syndrome)

This is a mild form of autosomal recessive SMA that appears after age 18 months. It

is characterized by slowly progressive proximal weakness. Most children with SMA

III can stand and walk but have trouble with motor skills, such as going up and down


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the stairs. The diseases progresses slowly, and the overall course is mild. Many

patients have normal life expectancies.

SMA Type IV (Adult-onset form)

Onset is typically in the mid 30s. the disease mimics the symptoms of type III.

Overall, the course of the disease is benign, and patients have a normal life

expectancy.

VII. Pathomechanism et Signs and Symptoms:

Signs et Symptoms

Often, weakness is first felt in the shoulder and leg muscles. Weakness gets worse

over time and eventually becomes severe.

Symptoms in an infant:

Breathing difficulty, leading to a lack of oxygen

Feeding difficulty (food may go into the windpipe instead of the stomach)

Floppy infant (poor muscle tone)

Lack of head control

Little movement

Weakness that gets worse

Symptoms in a child:

Frequent, increasingly severe respiratory infections

Nasal speech

Posture that gets worse

V. Differential Diagnosis:

Condition Differentialing S/Sx SimilaritiesAmyotrophic LateralSclerosis

ALS involves upper andlower motor neurons andpresents as an idiopathic,

Both SMA and ALS have astheir cardinal feature theloss of spinal motor

Mutation or Absence in the survival motor neuron gene

(telomeric SMN1 gene found in arm 5q - bands q11.2-13.3 )

Programmed Cell Death (Apoptosis)

Progressive Hypotonia or Muscle Weakness


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progressive degeneration ofanterior horn cells and theirassociated neurons,resulting in progressivemuscle weakness, atrophy,

and fasciculations.

Neurons.

Congenital MuscularDystrophy

Autosomal recessivediseases resulting in severeproximal weakness at birth(or within the first 12 mo oflife) that is either slowlyprogressive ornonprogressive.Contractures are common,and CNS abnormalities canoccur.

Both caused by faulty gene

Congenital Myopathies Hypotonia is the clinicalhallmark of congenitalmyopathies. It presents inthe neonatal period as headlag; lack of flexion of thehips, knees, and elbows;external rotation of the hips;diffuse weakness in facial,limb, and axial muscles;and reduced muscle mass.

Generalized muscleweakness and poor musclebulk.

Myasthenia Gravis A reduction in the number

of ACh receptors results ina characteristic pattern ofprogressively reducedmuscle strength. The bulbarmuscles are affected mostcommonly and mostseverely, but most patientsalso develop some degreeof fluctuating generalizedweakness.

progressive weakness,

muscle wasting, andmuscle fasciculations

Primary lateral sclerosis progressive, degenerative

disease of upper motorneurons characterized byprogressive spasticity (ie,stiffness). It affects thelower extremities, trunk,upper extremities, andbulbar muscles (usually inthat order).

VI. Diagnostic tools: 1. Genetic Testing

Although we do not fully understand how the gene abnormality produces the disease,

the discovery of the SMN gene has proved extremely helpful in both establishing a

diagnosis of SMA, and offering precise genetic counseling.


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confirms the diagnosis

2. Clinical Tests

Typically, the child with SMA Type I and II will exhibit his or her most dramatic

weakness in the proximal muscles of the legs and arms.

Most children with SMA lose their deep tendon reflexes (the reflexes physicians check

when they strike the knees or ankles with a rubber hammer).

3. Electromyography Testing (EMG)

4. Muscle Biopsy

VII. Medical management:

NO cure

Supportive treatment should be aimed at improving the patients' quality of life and

minimizing disability, particularly in patients with slow progression.

The goals are to maximize the patient's independence and quality of life at each stage

of the disease.

Respiratory muscle weakness - Assisted ventilation also can help children and adults

with different forms of SMA. Many physicians advise starting out with noninvasive

ventilation, which generally means that air (usually room air, not enriched with oxygen) is

delivered under pressure through a mask or mouthpiece. This kind of system comes in

many forms and can be used as many hours of the day and/or night as necessary. It can

easily be removed for eating, drinking and talking.

Swallowing muscle weakness - Babies with severe swallowing and sucking weakness

can be fed by alternative methods, such as a feeding tube, often called a gastrostomy tube

or g-tube. A feeding tube is a small, flexible tube, about the diameter of a pencil, that allows

liquid nutrition (homemade or commercially prepared) to enter the stomach directly,

bypassing the mouth, throat and esophagus.

VIII. Surgical management:

Surgical revision may provide stable correction of the spine, and early orthopedic

intervention may be indicated in patients in whom prolonged survival is anticipated. Hip


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subluxations and dislocations are common. Nonsurgical treatment is generally preferred

unless pain is severe, owing to the high rate of repeated dislocation.

Noninvasive ventilation and percutaneous gastrostomy reportedly improves the quality

of life with no effect on survival. These modalities may be most effective in prolonginglifespan in patients with slowly progressive disease, whereas they may provide comfort

care in rapidly progressive infantile forms.

If scoliosis develops in a patient with spinal muscular atrophy, spinal instrumentation

and fusion may be necessary. Some upper extremity function can be lost after fusion.

Tendon lengthenings may be needed to improve joint position.

IX. PT management:

Physical Therapy is the treatment of disease and injury by mechanical means such as

exercise, heat, light, massage and electricity.

Goals: Maximize function, mobility, safety, and comfort

Aquatic therapy is an excellent way to maintain mobility, strength, and flexibility.

PT assists you in walking, transfers from one place to another, exercise, pain relief and

education for you and your family.

Exercise: helps maintain joint movement (Maintaining the patient's joint mobility is very

important, because the goal is to decrease the incidence of contractures. Plantar flexion

contractures are the most common), mood elevation and improves sleep patterns.

Stretching: to preserve or increase flexibility

o Active

o Active assistedo Passive

Ankle-foot orthotics worn at night may help to provide prolonged, passive stretching to

prevent worsening of ankle plantar flexion contractures.

Strengthening: does not change the progression of the disease. Too much can actually

over fatigue the muscle. Active exercise within the limits of your disease in important to

maximize your ability and prevent disuse and contractures.

Avoid activities that cause muscle or joint pain and excessive fatigue either during orafter your exercise program. Energy conservation is needed so that you do not over

work body areas of increased weakness and cause overuse syndromes and more pain,

weakness etc.


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X. Prognosis:

There is no cure for SMA. Treatment consists of managing the symptoms and preventing

complications.

The prognosis is poor for babies with SMA Type I. Most die within the first two years, because

of respiratory problems and infections. For children with SMA Type II, the prognosis for life

expectancy or for independent standing or walking roughly correlates with how old they are

when they first begin to experience symptoms - older children tend to have less severe

symptoms Life expectancy is reduced but some individuals live into adolescence or young

adulthood. Children with type III disease may survive into early adulthood. However, people

with all forms of the disease have weakness and debility that gets worse over time. May beprone to respiratory infections but with care may have a normal lifespan.


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POLIOMYELITIS

I. Definition of Condition

Poliomyelitis is an acute infectious virus disease caused by the poliovirus,

characterized by fever, motor paralysis, and atrophy of skeletal muscles often withpermanent disability and deformity, and marked by inflammation of nerve cells in the

ventral horns of the spinal cord called also infantile paralysis, polio.

II. Etiology:

Poliomyelitis is a disease caused by infection with the poliovirus. A human enterovirus

and member of the family of Picornaviridae. Poliovirus is composed of an RNA genome

and a protein capsid. The viral particle is about 30 nanometres in diameter with icosahedralsymmetry. Because of its short genome and its simple composition, poliovirus is widely

regarded as the simplest significant virus.

The virus spreads by:

Direct person-to-person contact

Contact with infected mucus or phlegm from the nose or mouth

Contact with infected feces

The virus enters through the mouth and nose, multiplies in the throat and intestinal tract,

and then is absorbed and spread through the blood and lymph system. The time from being

infected with the virus to developing symptoms of disease (incubation) ranges from 5 - 35

days (average 7 - 14 days).

III. Epidemiology:

affects children > 5 y.o.

1 in 200 infections leads to irreversible paralysis. Paralysed, 5% to 10% die when

their breathing muscles become immobilized.

Polio cases have decreased by over 99% since 1988,

In 2013, only three countries (Afghanistan, Nigeria and Pakistan) remain polio-

endemic, down from more than 125 in 1988.

Children in all countries are at risk of contracting polio. Failure to eradicate polio

from these last remaining strongholds could result in as many as 200 000 new cases

every year, within 10 years, all over the world.

In most countries, the global effort has expanded capacities to tackle other

infectious diseases by building effective surveillance and immunization systems.


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IV. Classification

STAGES

1. Acute Stage

Variable incubation period

6-20 days (1-3 weeks)

Reflects virus ingestion & multiplication

Increased physical activity late in incubation period leads to poorer prognosis

Acute disease reflects viraemia

Varies from mild malaise to encephalomeningitis & paralysis

Children may have initial malaise & fever followed by several days of well -being

Then recurrence with sore throat, d iarrhoea & meningism

Older children & adults lack prodrome Spinal anterior horn cell involvement

Onset of patchy asymmetric paralysis

Spasm of opposing muscles produces pain

DTR disappear

Flexor posturing = Lie with curled up joints

Muscles tender t o palpation

Reflex spasm with stretching

No sensory changes

Bulbar motor nuclei involvement

Fulminant encephalitis

Speech & swallowing problems

Sudden respiratory failure from resp centre involvement

Clinical diagnosis with no laboratory tests

Cons idered infective for 4 weeks

2. Convalescent Stage

Starts 2 days after normal temp & cessation of paralytic disease

Continues for 2 years

Spontaneous improvement in muscle power

Most rapid in first 4/12

Almost complete after 6/12

Average improvement is 2 grades above assessment at 1/12 following onset

1 grade above assessment at 6/12

3. Chronic Stage


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AKA Stage of Residual Paralysis

After 2 years

No further recovery

Characteristic features

Limb bluish

Wasted

Deformed

Disease in childhood = shortened limb (hence LLD)

Limb has floppy feel

Normal sensation

If trunk affected then see scoliosis or respiratory insufficiency

Problems include Deformity due to unbalanced paralysis

Instability from balanced paralysis

Deformity contributed to by growth & worse in earlier disease

4. Post-Polio Syndrome

Return of:

Pain

Fatigue

Muscle weakness

Functional impairment

30 -35 years after original polio

Late onset > 10 years

Severe disease

Four extremities involved

Ventilator dependence

Hospitalisation during acute illness

Onset of 2 or more of following

-Fatigue -Muscle weakness -New weakness -New atrophy

-Functional loss -Cold intolerance -No other cause


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V. Pathomechanism et Signs and Symptoms:


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VI. Differential Diagnosis:

VII. Diagnostic Tools

1. Throat and stool culture

2. Urine culture3. Test for polio antibodies levels

4. Lumbar puncture or spinal tap : performed to collect a sample of cerebrospinal

fluid (CSF) for biochemical, microbiological, and cytological analysis, or very

Disease Similarities Rule-outGuillain-Barr syndrome Muscle contractions or

muscle spasms in the calf,neck, or backMuscle weakness that isonly on one side or worseon one side comes onquickly

And may go worst intoparalysis

loss of reflexes, andnumbness or tingling inyour arms, legs, face, andother parts of your body.

Spinal Cord lesions

urinate Muscle contractions ormuscle spasms in the calf,neck, or back

Medical Hx.

Neuropathies

spasm in any area of thebody

neckstiffness of the

back, arms, legs,abdomen

Physical trauma,repetitive injury,metabolic problems andexposure to toxins andsome drugs

Myasthenia Gravis Fluctuating muscleweakness andfatigue

Possitive acetylcholinereceptor antibodies

West nile virus infection Skin rashSwollen lymph glandsStiff neck

Disorientation or confusionStupor or comaTremors or muscle jerkingLack of coordinationEye pain


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rarely as a treatment ("therapeutic lumbar puncture") to relieve increased

intracranial pressure.

VIII. Medical Management

There is no cure for polio, only treatment to alleviate the symptoms. Heat and physical

therapy is used to stimulate the muscles and antispasmodic drugs are given to relax the

muscles. While this can improve mobility, it cannot reverse permanent polio paralysis.

Polio can be prevented through immunization. Polio vaccine, given multiple times,

almost always protects a child for life.

IX. Surgical management:

1. Hip and knee contractures of over 30

Souttars release involves the soft tissue release on the anterolateral aspect of the hip

joint, whereby the tensor fascia lata and gluteus maximus are released from their origins,

as they contribute to the formation of the iliotibial band.

Younts releas e involves reexcision of the thickened anterolateral fascia lata so that the

knee contracture is better corrected.

The subcutaneous method of division is very satisfactory for less severe contractures,

provided it is done correctly and as extensively as necessary. Care must be taken to avoid

damaging the femoral and popliteal arteries, as well as the common peroneal nerve. The

biceps, however, should always be divided under direct vision because of the risk of

damaging the adjacent lateral popliteal nerve.

2. Tendon transfer to reestablish muscle power

In selecting a tendon to transfer, the muscle should be sufficiently strong to supplement

the power of a paralyzed muscle. The nerve and blood supply of the transferred muscle

should be preserved in order to avoid iatrogenic weakness.

For efficiency, the transferred tendon should be securely attached (with tension) close

to the insertion of a paralyzed tendon and should be routed in a direct line between its

origin and the new insertion. The transferred tendon loses its power by one grade.

3. Muscle transplantation to replace a paralyzed muscle

In muscle transplant procedures, unlike in tendon transfer, both the origin and the

insertion of a muscle are detached along with its neurovascular pedicle. This procedure is


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not as popular as tendon transfer, because of the difficulty in finding a normal muscle to

transplant.

4. Arthrodesis

5. Limb lengthening6. Joint replacement surgery

X. PT management:

Physical therapy plays an important role in

rehabilitation for patients with poliomyelitis.

Patients with muscle paralysis benefit from

frequent passive range of motion (PROM)

and splinting of joints to prevent contracture

and joint ankylosis.

Chest physical therapy (CPT) helps

patients with bulbar involvement prevent any

pulmonary complications, such asatelectasis.

Frequent repositioning of paralyzedpatients helps to prevent bedsores.

Strengthening exercises should benonfatiguing. A specific suggestion is toexercise every other day, and the perceivedrate of exertion should be less than "veryhard." Loads should be held for only 4-5

seconds, and there should be a 10-second rest between bouts and a 5-minute restbetween sets. The patient should perform about 3 sets of 5-10 repetitions.

Electrical stimulation has been used to strengthen weakened muscles or to reeducatemuscles weakened through disuse, as well as to decrease pain.

For myofascial pain , consider heat, electrical stimulation, trigger point injections,stretching exercises, biofeedback, muscle relaxation exercises, or static magnetic fieldsfor trigger points.

For gait disturbances , assistive devices can be used, but sometimes patients refuse

because of the philosophy of "not giving in." Treatment also can involve limitation of

ambulation to shorter distances and the use of orthotics for joint protection.

Exercise therapy and training programs in PPS patients should be carefully

customized and planned by physiotherapists to avoid both overuse and disuse, and the

level of physical activity should be modified to decrease pain.


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XI. Prognosis:

People with minor illness and nonparalytic forms of polio recover completely, and most

people with major illness who were paralyzed also recover completely. Fewer than 25% of

people with polio are disabled for life.

Even though you can recover completely from polio symptoms, polio leaves behind

some damage. As you age, your nervous system may become less able to compensate for

the damage that polio caused, so symptoms may gradually reappear. This can happen 15

or 30 years after the polio infection was active. Recurring symptoms from polio are called

post-polio syndrome.


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