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
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
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