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ACUTE FLACCID PARALYSIS

• DEFINITION
sudden onset of weakness or paralysis over a
period of 15 days in a patient less 15 years of age
INVOLVEMENT

• Anterior horn cells


• Poliomyelitis
• Acute transverse myelitis

• Nerve fibres
• Postinfectious polyneuropathy (GBS
syndrome)
• Toxins----diphtheria, porphyria
INVOLVEMENT

• Neuromuscular junction
• Tick toxin
• Botulinum toxin
• Metabolic causes
• Periodic paralysis
• Muscular disease
• Myositis
GUILLIAN BARRE SYNDROME

DEF
it is an idiopathic, acquired, postinfectious
polyneuropathy
EPIDEMIOLOGY
annual incidence is 0.4 to 1.7/ 100000
male > female
any age however rare before one year
PATHOPHYSIOLOGY
• Immune mediated disease
• Follows a viral respiratory tract infection or a
gastrointestinal infection
• Bacteria share antigenic sites with axons & peripheral
nerve myelin sheaths or both
• Inflammation and demyelination with infiltration of
macrophages which penetrate the basement membrane
of schwann cells exposing the axons and causing focal
conduction block
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
EITIOLOGY
• Mycoplasma
• Hepatitis B
• CMV
• EBV
• Measles
• Mumps
• Echovirus
• Cocksakie virus
• Influenza virus
• Compylobacter jejuni
CLINICAL FEATURES
 Appear within 2 wks after 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 symmetrical beginning in the legs
and ascending to involve the arms, trunk, throat and
face
 Progression can occur rapidly in hours or days or
more slowly over weeks
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
Differentiation from spinal cord syndrome

Loss of arm reflexes


Absence of sensory level
Lack of spinal tenderness
Normal bowel and bladder function
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
DIAGNOSIS

Clinical
nerve conduction studies
slowing of nerve conduction
electromyogram
extensive fibrillation showing denervation
CSF
increased proteins with normal leukocytes during 2nd
week of illness
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
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
PROGNOSIS

– Mortality 3%
– Recovery
• 1 to 6 months, may take 12 months
• Delayed recovery may be followed by permanenent
neurological sequelea
D/D of acute flaccid paralysis
GB Syndrome Spinal cord poliomyelitis
syndrome
Eitiology Delayed Trasverse Poliovirus type
hypersesitivity. myelitis,spinal I,II,III
antibody mediated cord abscess,TB

History GI or URTI, 5 to Rapid progression Unimmunized,


14days preceding of symptoms URTI or GI
symptoms infection

Symptoms Symmetric weakness Back pain. Fever,.


in LL gradually Sensory loss meningismus,
ascending with below the level of muscle
parasthesias. normal lesion, sphincter tenderness,
bowel & bladder problems asymmetric
function weakness
Signs Symmetric flaccid Symmetric Assymmetric
weakness, sensations areflexia,sensory flaccid weakness,
intact, gradually loss below the sensations intact,
ascending level of lesion., muscle wasting
pain, bowel and
bladder
dysfunction

CSF findings Normal cell count Pleocytosis with Pleocytosis with


with raised protiens raised protiens raised protiens
2nd week of illness

EMG/NCS Signs of denervation, Normal initially NCS normal,


NCS shows delayed EMG denervation
conduction later

Course and Recovery in majority Depends on Permanent


prognosis within 12 months eitiology disability in 1%
cases