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ACUTE FLACCID PARALYSIS

Dr Shreedhar Paudel

May, 2009

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DEFINITION

Sudden onset of weakness or paralysis over a

period of 15 days in a patient less 15 years of age

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INVOLVEMENT

Anterior horn cells

Poliomyelitis

Acute transverse myelitis

Nerve fibres

Postinfectious polyneuropathy (GBS

syndrome)

Toxins----diphtheria, porphyria

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INVOLVEMENT

Neuromuscular junction

Tick toxin

Botulinum toxin

Metabolic causes

Periodic paralysis

Muscular disease

Myositis

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GUILLIAN BARRE SYNDROME

DEFINITION

It is an idiopathic, acquired, postinfectious

polyneuropathyEPIDEMIOLOGY

Annual incidence is 0.4 to 1.7/ 100000

Male > female

Any age however rare before one year

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PATHOPHYSIOLOGY

Inflammation causes leakage of proteins into the CSF

causing raised CSF proteins without pleocytosis

Can involve the peripheral nerves, cranial nerves, dorsal

roots, dorsal root ganglia & sympathetic chain

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EITIOLOGY

Mycoplasma

Hepatitis B

CMV

EBV Measles

Mumps

Echovirus

Cocksakie virus

Influenza virus

Campylobacter jejuni

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CLINICAL FEATURES

Appear within 2 wksafter onset of viral infections

C/O numbness or parasthesias in the hand and feet

followed by a heavy weak feeling in the legs

Followed by inability to walk The weakness is symmetricalbeginning in the legs

and ascending to involve the arms, trunk, throat and

face

Progression can occur rapidly in hours or days ormore slowly over weeks

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SIGNS

Marked flaccidity ---- hypotonia

Complete areflexia

Minimal signs of sensory loss

Progress to bulbar signs and respiratory insufficiency

Cranial nerve involvement

Autonomic dysfunction --- hypotension,hypertension, orthostatic hypotension, tachycardia,urinary retention or incontinence, stool retention,

episodes of abnormal sweating, flushing,vasoconstriction

Intact sensations

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CLINICAL VARIANTS

Polyneuritis cranialis

Cranial nerve involvement

Miller fisher syndrome Ophthalmoplegia, ataxia, areflexia

Chronic progressive GBS

Symptoms persisting more than 6 weeks

Chronic relapsing GBS

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DIAGNOSIS

Clinical

Nerve conduction studies

slowing of nerve conduction

Electromyogram

extensive fibrillation showing denervation

CSFincreased proteins with normal leukocytes during 2nd

week of illness

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MANAGEMENT

SUPPORTIVE

Close monitoring of vital signs

Nursing care Repeated spirometries

Bowel and bladder care

Tube feeding

Care for bed sores Ventilatory support if required

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MANAGEMENT

SPECIFIC

Steroids-----2mg/kg for 2 weeks

Plasmapheresis-----to remove antibodies I/V immunoglobulins-----400mg/kg for 5 days or

1gm/kg for 2 days

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PROGNOSIS

Mortality 3%

Recovery

1 to 6 months, may take 12 months Delayed recovery may be followed by permanenent

neurological sequelea

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D/D of acute flaccid paralysis

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GB Syndrome Spinal cord

syndrome

poliomyelitis

Eitiology Delayed

hypersesitivity.antibody mediated

Trasverse

myelitis,spinalcord abscess,TB

Poliovirus type

I,II,III

History GI or URTI, 5 to

14days precedingsymptoms

Rapid progression

of symptoms

Unimmunized,

URTI or GIinfection

Symptoms Symmetric weakness

in LL gradually

ascending with

parasthesias. normal

bowel & bladder

function

Back pain.

Sensory loss

below the level of

lesion, sphincter

problems

Fever,.

meningism,

muscle

tenderness,

asymmetric

weakness

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Signs Symmetric flaccid

weakness, sensations

intact, gradually

ascending

Symmetric

areflexia,sensory

loss below the

level of lesion.,pain, bowel and

bladder

dysfunction

Assymmetric

flaccid weakness,

sensations intact,

muscle wasting

CSF findings Normal cell count

with raised protiens

2nd week of illness

Pleocytosis with

raised protiens

Pleocytosis with

raised protiens

EMG/NCS Signs of denervation,

NCS shows delayed

conduction

Normal initially NCS normal,

EMG denervation

later

Course and

prognosis

Recovery in majority

within 12 months

Depends on

eitiology

Permanent

disability in 1%

cases