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ACUTE FLACCID PARALYSIS
• GULLAIN BARRE SYNDROME
• TRAUMATIC NEURITIS
• Common cause of AFP in children
• AUTO IMMUNE
• Rapidly progressive
• Symmetric polyradiculoneuropathy
• Occur at any age
• 2/3 rd patient have an infection within 6 week
prior to symptom onset- URTI / gastroenteritis
CLINICAL FEATURES
• A/c onset of symmetrical ascending weakness
• More in distal muscles
• Distal parasthesia & pain precede muscle weakness
• Facial and bulbar weakness commonly develop
• Involvement of respiratory muscles – ¼ th cases –
ventilatory support
• Deep tendon reflexes are diminished
• Hypotonia
• Sensory involvement
• Dysautonomia
• Tachycardia, arrythmia , bladder dysfunction,
labile blood pressure, impaired thermoregulation
• Weakness reaches a max in 4 wks- gradual
recovery over weeks to month
SUB TYPES
• a/c inflammatory demyelinating
polyradiculoneuropathy
• a/c motor axonal neuropathy
• a/c motor and sensory neuropathy
• a/c sensory neuropathy
• a/c pandysautonomia
• Miller fisher syndrome
• Miller fisher syndrome
• ophthalmological abnormalities
• Ataxia
• areflexia
INVESTIGATION
• C/F
• ELECTROPHYSIOLOGICAL STUDIES
• CSF examination
• CSF protein is raised
• CSF white cell count is
normal(albumincytologic dissociation) or
below 50 cells / mm₃
• Electrophysiological studies and CSF study nl
– first week of illness
• Eletrophysiology
• Absent F responses or H reflexes ,
Reduced compound muscle action potential
or sensory nerve action potential - axonal
forms
• Prolonged distal latencies, reduced
conduction velocities, abnormal temporal
dispersion, &conduction blocks-
demyelinating types
TREATMENT
• IMMUNOTHERAPY – IVIG 2g/kg over 2-5 days
• Plasma exchanges– within 2-4 wks of onset
• Indicated Non ambulatory patient
• Sev d/s , IVIG therapy(if initiated with in 2 wks
from onset) hastens recovery as much as PE
• General supportive care
• Cardio respiratory care
• Physical therapy
• Nutritional management
• Management of neuropathic pain
• Care of bladder and bowel
• Prevention of DVT
TRAUMATIC NEURITIS
TRAUMATIC NEURITIS
• Defined as inflammation of nerve after injury
• Progression to complete paralysis is hours to 4
days
• No onset of fever
• Flaccidity is acute and asymmetric
• Hypotonia and deep tendon reflexes are
diminished
• Pain in gluteal region
• No cranial nerve invovement
• CSF is normal
• No bladder or bowel involvement
• Nerve conduction velocity at 3 week is
abnormal
• Sequelae at 3 months – moderate atropy in
affected limb
GBS TRAUMATIC NEURITIS
fever May hav prodromal illness absent
symmetry Symmetrical asymmetric
sensations variable May be impaired in the
distribution of affected nerve
Respiratory insufficiency May be present absent
Cranial nerves Usually affected absent
Radicular signs present absent
Bladder bowel complaints Transient ,d/t autonomic
dysfunction
absent
Nerve conduction abnormal abnormal
CSF Albumino cytologic
dissociation
normal
M RI spine Usually normal normal
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Guillen barre syndrome

  • 2. • GULLAIN BARRE SYNDROME • TRAUMATIC NEURITIS
  • 3.
  • 4. • Common cause of AFP in children • AUTO IMMUNE • Rapidly progressive • Symmetric polyradiculoneuropathy • Occur at any age • 2/3 rd patient have an infection within 6 week prior to symptom onset- URTI / gastroenteritis
  • 5.
  • 6. CLINICAL FEATURES • A/c onset of symmetrical ascending weakness • More in distal muscles • Distal parasthesia & pain precede muscle weakness • Facial and bulbar weakness commonly develop • Involvement of respiratory muscles – ¼ th cases – ventilatory support
  • 7. • Deep tendon reflexes are diminished • Hypotonia • Sensory involvement • Dysautonomia • Tachycardia, arrythmia , bladder dysfunction, labile blood pressure, impaired thermoregulation • Weakness reaches a max in 4 wks- gradual recovery over weeks to month
  • 8. SUB TYPES • a/c inflammatory demyelinating polyradiculoneuropathy • a/c motor axonal neuropathy • a/c motor and sensory neuropathy • a/c sensory neuropathy • a/c pandysautonomia • Miller fisher syndrome
  • 9. • Miller fisher syndrome • ophthalmological abnormalities • Ataxia • areflexia
  • 10. INVESTIGATION • C/F • ELECTROPHYSIOLOGICAL STUDIES • CSF examination
  • 11. • CSF protein is raised • CSF white cell count is normal(albumincytologic dissociation) or below 50 cells / mm₃ • Electrophysiological studies and CSF study nl – first week of illness
  • 12. • Eletrophysiology • Absent F responses or H reflexes , Reduced compound muscle action potential or sensory nerve action potential - axonal forms • Prolonged distal latencies, reduced conduction velocities, abnormal temporal dispersion, &conduction blocks- demyelinating types
  • 13. TREATMENT • IMMUNOTHERAPY – IVIG 2g/kg over 2-5 days • Plasma exchanges– within 2-4 wks of onset • Indicated Non ambulatory patient • Sev d/s , IVIG therapy(if initiated with in 2 wks from onset) hastens recovery as much as PE
  • 14. • General supportive care • Cardio respiratory care • Physical therapy • Nutritional management • Management of neuropathic pain • Care of bladder and bowel • Prevention of DVT
  • 15.
  • 17. TRAUMATIC NEURITIS • Defined as inflammation of nerve after injury • Progression to complete paralysis is hours to 4 days • No onset of fever • Flaccidity is acute and asymmetric • Hypotonia and deep tendon reflexes are diminished • Pain in gluteal region • No cranial nerve invovement
  • 18. • CSF is normal • No bladder or bowel involvement • Nerve conduction velocity at 3 week is abnormal • Sequelae at 3 months – moderate atropy in affected limb
  • 19. GBS TRAUMATIC NEURITIS fever May hav prodromal illness absent symmetry Symmetrical asymmetric sensations variable May be impaired in the distribution of affected nerve Respiratory insufficiency May be present absent Cranial nerves Usually affected absent Radicular signs present absent Bladder bowel complaints Transient ,d/t autonomic dysfunction absent Nerve conduction abnormal abnormal CSF Albumino cytologic dissociation normal M RI spine Usually normal normal