1. Acute flaccid paralysis (AFP) is defined as sudden onset of weakness or paralysis over 15 days in patients under 15 years old. It suggests involvement of the lower motor neuron complex. 2. Common causes of AFP include poliomyelitis, Guillain-Barré syndrome, transverse myelitis, botulism, and non-polio enteroviruses. Clinical features and investigations can help differentiate between these causes. 3. Treatment depends on the underlying etiology but may include supportive care, IV immunoglobulin, plasmapheresis, and corticosteroids. Prognosis ranges from full recovery to residual deficits or death, depending on the cause and extent of

1. ACUTE FLACCID PARALYSIS
AFP
Dr. Mohamed I. Abunada
Head of Pediatric
Neurology Department
Dr. Al rantisi Specialized
children Hospital

2. DEFINITION
• Sudden onset of weakness or paralysis over a
period of 15 days in a patient aged less than
15 years age
• Flaccid paralysis evolving over hours or a few
days
• suggests involvement of the lower motor
neuron complex.

3.  Muscle contraction results from a chain of events that
=begins with a nerve impulse
=traveling in the upper motor neuron from the
(cerebral cortex in the brain to the spinal cord)
=the nerve impulse then
=travels in the lower motor neuron from the
(spinal cord to the neuromuscular junction)
=then stimulation of the muscles occurs.

5. Upper motor neuron disease
vs
Lower motor neuron disease
Spastic paralysis
• U.M.N.L (the neurons in
the brain and spinal cord
that activate the motor
neurons)
• hyperactive DTRs
• Clonus
• Positive Babinski
• absence of muscle
atrophy
Flaccid paralysis
• L.M.N.L(spinal & cranial
motor neuron that directly
innervate the muscle)
• Muscle wasting is a
prominent feature.
• Hypotonia
• Hyporeflexia

6. Syndromes Presenting as AFP (DD)
Anterior horn cells AHC (spinal cord)
 acute poliomyelitis
 acute transverse myelitis
Peripheral Nerves
 roots: GBS (post-infectious)
 toxins: Diphteria, porphyria
N-M junction:
botulinum toxin , tick toxin
Metabolic: Periodic paralysis
Muscular: myositis (rare)
A lesion compressing the spinal cord must be ruled out.

7. ACUTE FLACCID PARALYSIS
AFP
Asymmetric
Polio
Non
polio
entero
viruses
Pseudo-
paralysis
Symmetric
GBS
Acute
spinal
cord
compr
ession
Transverse
Mylitis
Botulism

8. Features assisting diagnosis
• Age.
• A history of preceding or warning illness.
• A history of trauma.
• The presence (at time of paralysis) of fever.
• Rapidity of progression.
• Cranial nerve findings, and sensory findings.
• The Examination should include a search of fracture , focal
tenderness or swelling and painful limping gait.
• The examination may show UMNL signs
 increased reflexes
 Hypertonicity
 a positive Babinski sign.
• Laboratory findings occasionally are diagnostic

9. Imaging&Neurophysiology
 NERVE CONDUCTION VELOCITY (NCV). Neuropathies of
various types are detected by decreased conduction.
 ELECTROMYOGRAPHY (EMG). Characteristic EMG patterns
distinguish denervation from myopathic involvement.
 CSF exam: in suspected CNS infection or GBS
 MRI is the study of choice to image the spinal cord or nerve
roots & plexus (e.g., brachial).
 CK (creatine kinase)
 Enzymes are released by damaged or degenerating muscle
fibers.
 Many diseases of the motor unit may not be associated
with elevated enzymes.

10. Guillain-Barre Syndrome (GBS)
Barre
Gullian Post-infectious
acute, rapidly progressing
ascending
 potentially fatal form of
polyneuritis
involving mainly motor but
sometimes also sensory and
autonomic nerves
 also known as: Acute
inflammatory demyelinating
polyneuropathy (AIDP)

11. Epidemiology
The most common cause of AFP among infants(2
cases per 100,000 population).
At an age usually in children over 4-9 years
Sex : any ( male > female)
follows infection by 10 days
GIT infection
 Campylobacter jejuni (26-41%)
 Cytomegalovirus
Respiratory tract infection
Mycoplasma pneumoniae
Vaccines
– Rabies
– Avian-flu influenza

12. Pathogenesis
Molecular mimicry
Cross-reactive immune
attack by host
Antibody & T cell which
are directed against
the pathogen & nerve
components (myelin to
cause
demyelination).

13. Clinical Features
Weakness
o Onset is gradual and progresses over weeks
o Lower extremities (unable/refusal to walk)  trunks 
upper limbs  bulbar muscles  flaccid tetraplegia =
Landry Ascending Paralysis
o Proximal and distal muscles are involved relatively
symmetrically, but asymmetry is found in 9% of patient
Muscle tenderness – At the onset
Paraesthesias – in some cases
Areflexia (83%)

14. Clinical Features
Bulbar involvement (50%)
o Dysphagia and facial weakness – signs of impending
respiratory failure
Cranial nerve involvement (50%)
o Facial nerve , Oculomotor nerve
Autonomic involvement
o Lability of blood pressure
o Profound bradycardia
o Occasional asystole
o Urinary retention or incontinence (20% of cases)
Miller-Fisher syndrome
o External ophtalmoplegia
o ataxia
o areflexia

15. Investigations
Electromyography
 Motor nerve conduction velocities are reduced
 Evidence of acute denervation of muscle
Lumbar puncture – cerebrospinal fluid (CSF)
 Elevation of CSF protein (more than twice upper limit of normal)
 Cell content of CSF is normal (<10 cells/mm³)
 Glucose level normal
 Bacterial and viral culture is negative

16. Treatment
o Intravenous immunoglobulin (IVIG), 2 gm/kg/day
administered for 2 or 5 days
o Plasmapheresis, steroids, if IVIG is ineffective
o Supportive care, such as respiratory support,
prevention of decubiti in children with flaccid
tetraplegia, and treatment of secondary bacterial
infections

17. Prognosis
Spontaneous recovery begins within 2–3
weeks.
Most regain normal muscular function
Improvement usually follows a gradient
inverse to the direction of involvement.
Bulbar and respiratory muscle
involvement may lead to death if the
syndrome is not recognized and treated

18. Poliomyelitis
Polio= gray matter
Myelitis= inflammation of the spinal
cord
• First described by
*Michael Underwood* in 1789
• First outbreak described in U.S. in
1843
•21,000 paralytic cases reported in the
U. S. in 1952
• Most affects children < the age of 5
years in developing tropical countries.
• Global eradication in near future

19. Poliomyelitis
It is a viral infection Enterovirus (RNA)
Rapidly inactivated by heat, formaldehyde,
chlorine, ultraviolet light
It is contagious: usually spread from person to
person.
Incubation period ranges from 6 to 20 days
Only harmful to humans
Virus localized in the anterior horn cells of the
spinal cord and certain brain steam motor nuclei.

21. Poliomyelitis Pathogenesis
Entry into mouth
Replication in GI tract, local
lymphatics
Hematologic spread to lymphatics
and CNS
Viral spread along nerve fibers
Destruction of motor neurons
(AHCs)
Destruction of the spinal cord
occurs focally and within 3 - 6days .

22. Clinical Presentation
Acute stage: generally lasts 7 to 10 days.
fever
pharyngitis
headache
anorexia
nausea
vomiting.
Illness may progress to aseptic meningitis and
meningioencephalitis in 1% to 4% of patients.
 Symptoms range from mild malaise to generalized
encephalomyelitis with widespread paralysis.

23. Clinical course
 Paralytic disease occurs 0.1% to 1% of those who become
infected with the polio virus.
 Hyperesthesia or paresthesia in the extremities and
muscular pain is common
 Paralysis of the respiratory muscles or from cardiac arrest if
the neurons in the medulla oblongata are destroyed.
Paralysis occurs twice as often in the lower extremity as in
upper extremity.

24. Poliomyelitis-Prognosis
Patients have some or
full recovery from
paralysis, most clinical
recovery occurs during
the 1 month and almost
complete within 6
months.
Limited recovery may
occur for about 2 years.

25. Treatment in the acute stage
Bed rest, analgesics, hot packs, and anatomical
positioning of the limbs
Close monitoring of respiratory and
cardiovascular functioning is essential during
the acute stage of poliomyelitis along with fever
control and pain relievers for muscle spasms.
Mechanical ventilation, respiratory therapy may
be needed depending of the severity of
patients.

26. Physiotherapy
gentle passive ROM exercises of all joints
Physical therapy is recommended for full
recovery.
Passive stretching exercises for mild to moderate
contractures
Surgical release of tight fascia and lengthening of
tendons may be necessary for contractures
persisting longer than 6 months.
Orthoses should be used until no further
recovery is anticipated.

27. Prevention & Eradication

30. The National Immunization Schedule in
Palestine
The VaccineAge
Hep.B1BCG1 d.
IPV1Hep.B21m.
DPT1OPV1IPV22m.
DPT2OPV24m.
DPT3OPV3Hep.B36m.
Measles9m.
DPT4OPV412m.
MMR15m
DTOPV6y.
Rubella
(girls)
12y.
d T15y.

31. Non-polio enteroviruses
Coxsackie viruses and echo viruses can affect
the AHCs and cause AFP.
Paralysis is usually mild , not massive and
transient.

32. Pseudoparalysis
• Not a true paralysis
• May follow unrecognized trauma (fracture,
sprain, contusion), toxic synovitis of hip or
knee or acute osteomylitis
• Careful exam show focal tenderness
• Usually painful limping gait.
• Neuro exam is free.

33. Botulism
• It’s a toxic neuromuscular blockade
caused by Clostridium botulinum
(anaerobic gram positive)
• According to the type of infection,
there is 3 types
1- infant B. due to exposure to soil,
honey
2- food-borne B. due to ingestion
improperly home preserved foods
containing the toxins
3- Wound B. due to wound
contamination with the organism

35. Botulism
• All three types of botulism result in
symmetric descending flaccid
paralysis of motor and autonomic
nerves always beginning with the
cranial nerves.
• These symptoms are preceded by
constipation in cases of infant
botulism.
 If left untreated - paralysis of
respiratory muscles as well as the arms
and legs.
 Respiratory paralysis is the most
common cause of death in botulism
cases.

36. Treatment
• Antitoxin can halt the progress of symptoms if
administered early to victims of food and
wound botulism.
• Antitoxin is not given to victims of infant
botulism because when this is diagnosed it is
generally too late for the antitoxin to do any
good.

37. Transverse Mylitis
• The 2nd most common cause of symmetric AFP
• It’s a segmental dysfunction of spinal cord without
evidence of spinal cord compression
• The cause is either a direct viral infection or an
autoimmune disease.
• Paralysis is usually affect only LL (Paraplegia). rare
above 5th cervical segment lead to quadriplegia .
• Initially flaccid but gradual change to spasticity over
few weeks
• Sensory loss (with sensory level on the trunk)and
autonomic disturbance (urinary retention and stool
incontinence) are usually present

39. treatment
• Intravenous Steroids
 Although there are no clinical trials that support a
unique approach
 it is well recognized as a standard of care to give
high-dose intravenous methyl-prednisolone for 3-5 days
 The decision to offer continued steroids or add a new
treatment is often based on the clinical course and MRI
appearance at the end of 5 days of steroids.
• Plasma Electrophoresis
 mostly
• Prolonged course
• Complete recovery in 60% of cases

40. Acute spinal cord compression
• Trauma to the back
• Spinal epidural abscess
• Vascular anomalies of the cord
• Spinal cord tumors.
Clinically difficult to differentiate from
Transverse Mylitis
CT scan of the spine or MRI are sensitive and
can show the nature of obstruction

41. Prognosis & complications of AFP
According to cause for example:
Poliomyelitis
Respiratory, death, Limb atrophy.
Guillain- Barre Syndrome:
Respiratory, autonomic crises, residual weakness,
death.
Acute transverse myelitis
Residual deficits include bowel and bladder
dysfunction & weakness in the lower extremities