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Nazar deen FAROOQI
IPM&R,DUHS
   Landrys ascending paralysis.
   Acute inflammatory demyleniating poly
    neuropathy (AIDP)
   Acute idiopathic polyneuritis
   French polio
   Landry Guillain Barre syndrome.
   GBS is an autoimmune disease marked by an acute inflammation
    of the peripheral nerves effecting arms and legs.
   It is characterized by weakness and numbness or tingling in legs,
    arms, and possible loss of movement in upper body and face.
   Involves destruction of myelin sheath surrounding largest most
    myelinated sensory motor fiber.
   Resulted in disruption of proprioception and weakness of limbs.
 In more severe cases complete paralysis and breathing difficulty
  noted.
 In most cases GBS follows recent viral and bacterial infections.
   No clear cause.
   Neither contagious nor hereditary.
   Possible vaccine causal link.
   Autoimmune----body produces antibodies that
    damages myelin sheath.
   In about half of all cases the onset of symdrom follows
    viral or bacterial infections.
   Camphylobacteriosis---usually eating uncooked
    poultry.
   Influenza
   Gastrointestinal viral infection.
   HIV
•Porphyrin----rare disease of RBC.

•Viral hepatitis.
• Epidural anesthesia.

•Thrombolytic agents.

•Small number of cases have been known to occur after minor surgeries

• GBS has been associated with systemic processes like
•Hodgkin’s disease.
•SLE
•Sarcoidosis
•EBV, CMV,
•Lyme disease.
•Mycoplasma.
 Hypotonia and areflexia (absence of reflexes).
 Numbness and tingling in hands and feet Distal
  progression:
 Muscle weakness
 Diminished reflexes and proprioception,
  decreased sensation,
 For some progresses to trunk, face, and cranial
  nerves, resulting in difficulty swallowing,
  chewing, speaking, and facial expressions
 Deep, aching pain/hypersensitivity to touch
 Respiratory/cardiac dysfunction and failure.
•The initial symptoms are SENSORY CHANGES: paresthesia,
numbness; usually mild; 70% pts have sensory abnormalities.
•burning,tingling,shocklike,persistent in 5-10%
•WEAKNESS- ascending and symmetrical, lower limbs
involved first, proximal muscles involved earlier; develops
acutely and progresses; wide variations in severity.
•AUTONOMIC CHANGES: tachycardia, bradycardia, facial
flushing, paroxysmal HTN, orthostatic hypotension,
anhidrosis,diaphoresis, urinary retention, ileus, dizziness;
more common if severe weakness or respiratory failure.
 It is characterized by focal segmental
  demyelination with perivascular and endoneurial
  infiltrates of lymphocytes and monocytes or
  macrophages.
 These lesions are scattered throughout the
  nerves, nerve roots. And cranial nerves.
 In particularly severe lesions, there is both
  axonal degeneration and segmental
  demyelination
 During recovery, remyelination occurs, but the
  lymphocytic infiltrates may persist.
   Affects 2/100000 annually.

   None-discriminatory, can effects persons of
    any gender, age.
   80% experience complete recovery.
   Recovery may last for 2 months to 2 years, It has three distinct
    phases.
   Acute (4 weeks) initial rapid onset of symptoms.
   Plateau (few days to few weeks). Symptoms neither worsen nor
    improve.
   Recovery (gradual improvement or recovery is accompanied by
    pain and tingling in limbs.
   Childrens makes better recovery than adults.
   Recent studies on the disease demonstrate that approximately
    80% patients have Myelin loss while 20% have Axon loss.
   5% dies because of cardiopulmonary complications.
   GBS is difficult to diagnose because of
    symptoms varying and due to no specific
    cause.
   Physical and neurological examination.
   Lumber puncture (high protein contents is
    demonstrated in CSF).
   NCS (showing flowing o nerve conduction in
    nerves root and in peripheral nerves
   EMG (Ineffective tool)
   Limited physical mobility.
   Inability to engage in meaningful occupation
    because of pain.
   Extreme muscle weakness in arms and legs.
   Fatigue.
   Sensory functions impaired.
   Mental confusion.
   Medical
   GBS should be considered as medical
    emergency.
   Intravenous immunoglobulin therapy.
   It prevents immune system from further
    attacking Schwann cells and myelin sheath,
    brocking receptor and microphage
   Plasmapheresis
   Filters blood plasma to remove antibodies. It can
    shorten the course, alleviates symptoms in
    prevent paralysis.
•Corticosteroids
•It inhibit inflammation associated with symptoms.

• Muscle relaxant/ anticonvulsant / pain killer.
   Before recovery begins (PROM)
   After symptoms subside (ARON)
   Positioning .
   Active muscle strengthening.
   Mobility skills. Training with adaptive devices
    such as wheel chairs or braces.
   Hydrotherapy. Whirlpool hydrotherapy may
    release pain and useful in retraining the
    movements of effected limbs.
   Counseling. To feel positive about their disease.
G ui llain- barre syndrome nazar

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G ui llain- barre syndrome nazar

  • 1. COMPILED BY Nazar deen FAROOQI IPM&R,DUHS
  • 2. Landrys ascending paralysis.  Acute inflammatory demyleniating poly neuropathy (AIDP)  Acute idiopathic polyneuritis  French polio  Landry Guillain Barre syndrome.
  • 3. GBS is an autoimmune disease marked by an acute inflammation of the peripheral nerves effecting arms and legs.  It is characterized by weakness and numbness or tingling in legs, arms, and possible loss of movement in upper body and face.  Involves destruction of myelin sheath surrounding largest most myelinated sensory motor fiber.  Resulted in disruption of proprioception and weakness of limbs.  In more severe cases complete paralysis and breathing difficulty noted.  In most cases GBS follows recent viral and bacterial infections.
  • 4. No clear cause.  Neither contagious nor hereditary.  Possible vaccine causal link.  Autoimmune----body produces antibodies that damages myelin sheath.  In about half of all cases the onset of symdrom follows viral or bacterial infections.  Camphylobacteriosis---usually eating uncooked poultry.  Influenza  Gastrointestinal viral infection.  HIV
  • 5. •Porphyrin----rare disease of RBC. •Viral hepatitis. • Epidural anesthesia. •Thrombolytic agents. •Small number of cases have been known to occur after minor surgeries • GBS has been associated with systemic processes like •Hodgkin’s disease. •SLE •Sarcoidosis •EBV, CMV, •Lyme disease. •Mycoplasma.
  • 6.  Hypotonia and areflexia (absence of reflexes).  Numbness and tingling in hands and feet Distal progression:  Muscle weakness  Diminished reflexes and proprioception, decreased sensation,  For some progresses to trunk, face, and cranial nerves, resulting in difficulty swallowing, chewing, speaking, and facial expressions  Deep, aching pain/hypersensitivity to touch  Respiratory/cardiac dysfunction and failure.
  • 7. •The initial symptoms are SENSORY CHANGES: paresthesia, numbness; usually mild; 70% pts have sensory abnormalities. •burning,tingling,shocklike,persistent in 5-10% •WEAKNESS- ascending and symmetrical, lower limbs involved first, proximal muscles involved earlier; develops acutely and progresses; wide variations in severity. •AUTONOMIC CHANGES: tachycardia, bradycardia, facial flushing, paroxysmal HTN, orthostatic hypotension, anhidrosis,diaphoresis, urinary retention, ileus, dizziness; more common if severe weakness or respiratory failure.
  • 8.  It is characterized by focal segmental demyelination with perivascular and endoneurial infiltrates of lymphocytes and monocytes or macrophages.  These lesions are scattered throughout the nerves, nerve roots. And cranial nerves.  In particularly severe lesions, there is both axonal degeneration and segmental demyelination  During recovery, remyelination occurs, but the lymphocytic infiltrates may persist.
  • 9. Affects 2/100000 annually.  None-discriminatory, can effects persons of any gender, age.
  • 10. 80% experience complete recovery.  Recovery may last for 2 months to 2 years, It has three distinct phases.  Acute (4 weeks) initial rapid onset of symptoms.  Plateau (few days to few weeks). Symptoms neither worsen nor improve.  Recovery (gradual improvement or recovery is accompanied by pain and tingling in limbs.  Childrens makes better recovery than adults.  Recent studies on the disease demonstrate that approximately 80% patients have Myelin loss while 20% have Axon loss.  5% dies because of cardiopulmonary complications.
  • 11. GBS is difficult to diagnose because of symptoms varying and due to no specific cause.  Physical and neurological examination.  Lumber puncture (high protein contents is demonstrated in CSF).  NCS (showing flowing o nerve conduction in nerves root and in peripheral nerves  EMG (Ineffective tool)
  • 12. Limited physical mobility.  Inability to engage in meaningful occupation because of pain.  Extreme muscle weakness in arms and legs.  Fatigue.  Sensory functions impaired.  Mental confusion.
  • 13. Medical  GBS should be considered as medical emergency.  Intravenous immunoglobulin therapy.  It prevents immune system from further attacking Schwann cells and myelin sheath, brocking receptor and microphage  Plasmapheresis  Filters blood plasma to remove antibodies. It can shorten the course, alleviates symptoms in prevent paralysis.
  • 14. •Corticosteroids •It inhibit inflammation associated with symptoms. • Muscle relaxant/ anticonvulsant / pain killer.
  • 15. Before recovery begins (PROM)  After symptoms subside (ARON)  Positioning .  Active muscle strengthening.  Mobility skills. Training with adaptive devices such as wheel chairs or braces.  Hydrotherapy. Whirlpool hydrotherapy may release pain and useful in retraining the movements of effected limbs.  Counseling. To feel positive about their disease.