G ui llain- barre syndrome nazar
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G ui llain- barre syndrome nazar






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G ui llain- barre syndrome nazar G ui llain- barre syndrome nazar Presentation Transcript

  •  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 limbsinvolved first, proximal muscles involved earlier; developsacutely and progresses; wide variations in severity.•AUTONOMIC CHANGES: tachycardia, bradycardia, facialflushing, 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.