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GB Pathology
- autoimmue response leads to demyelination of nerve fibers which results in inflammation
- slowed nerve conduction
- axons are usually preserved
- 2-3 after attack Schwann cells recover
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GB Clinical Feature
- usually begins in LE and effects them more
- ascending paraylsis
- motor involvement worse than sensory
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Why can GB be dangerous
- If if affects the ANS and reaches the phrenic nerve that controls the diaphragm and respiration
- 30% of pts
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Signs of Cranial Nerve Involvement
- problems swallowing(dsyphagia)
- lack of facial expression
- dysarthria
- diplopia
- Bulbar palsy (cranial nerve paralysis)
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Pain
- is severe and very common
- muscle belly pain (myalgia)
- hard to manage
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Plasmaphoresis
- blood is removed from the body, only red and white cells are returned
- this removes the immune factors in the plasma that cause the disease
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Immunoglobulins
given intravenously is useful to modulate the severity of the disease
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Prognosis
- 2.6% mortality
- 80% of pts recover after 1 year but not always fully
- recovery occurs opposite of onset
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Acute
- symptoms appear and worsen
- last up to 6 weeks
- have: paresthesias, motor areaflexia, and weakness is all limbs
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Plateau
- symptoms stay the same
- last up to 4 weeks
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Recovery
- begins when improvement starts
- takes months to years
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PT in Acute Stage
- monitor vitals
- PROM
- postioning
- gentle chest stretching
- cradle garments snug
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PT in Plateau
- upright positioning when resp & ANS are stable
- heat maybe allowed to help with pain
- continue from acute stage
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PT in Recovery
- Return of mm strength begins
- careful strengthening programs
- continue to monitor, splint, and TT
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Exercise for GB
- Short periods of non fatiguing
- advance intensity after 1 wk
- improve function vs. solely improving strength
- bedrest if deteriorate
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