Guillen barre syndrome

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ACUTE FLACCID PARALYSIS

Transcript of Guillen barre syndrome

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ACUTE FLACCID PARALYSIS

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• GULLAIN BARRE SYNDROME

• TRAUMATIC NEURITIS

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• 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

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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

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• 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

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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

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• Miller fisher syndrome

• ophthalmological abnormalities • Ataxia • areflexia

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INVESTIGATION

• C/F • ELECTROPHYSIOLOGICAL STUDIES• CSF examination

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• 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

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• 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

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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

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• General supportive care

• Cardio respiratory care• Physical therapy• Nutritional management• Management of neuropathic pain• Care of bladder and bowel• Prevention of DVT

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TRAUMATIC NEURITIS

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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

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• 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

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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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