GBS/MG Flashcards
(17 cards)
What is GBS
acute demyelination of cranial nerves and peripheral nerves/nerve roots
GBS etiology
Etiology: unknown; autoimmune mediated; usually occurs after recovery from an infectious illness (respiratory or gastrointestinal)
rapid onset, progressive - worst sis in first 2 weeks
what is the sudden progression of GBS calles
acute inflammatory demyelinating polyneuropathy (AIDP)
GBS prognosis
most people fully recover
signs and symptoms of GBS
sensory loss, paresthesias (tingling/burning)
motor paresis; relative symmetrical distribution; distal to proximal
dysarthria, dysphagia, diplopia, facial weakness
complications of GBS
respiratory impairment
auonomic instability
pain: myalgia
risk of pneumonia
prolongs hospitalizations and immobility (DVT, skin breakdown,, contractures)
relapse rare
medical Dx and Tx
lumbar puncture - elevated almbimin
NCV - delays in latency
EMG - decreased amplitude
Tx - plasmapheresis
IVIG
GBS PT exam
cardiac and respiratory status, vital signs
cranial nerves (7,9,19,11,12)
reflexes
motor strength
sensation
functional status
PT treatment: GBS
Maintain respiratory function
Prevent indirect impairments- PROM, positioning, skin care
Prevent injury to denervated muscles- bracing, splinting, positioning
Muscle reeducation, moderate exercise program (active assist, AROM, progress to resistive with recovery, functional training as recovery progresses)
Patient and family education
teach energy conservation techniques, activity pacing; avoid overuse and fatigue!!
peripheral nerve disorder: poliomyelitis postpolio syndrome (PPS)
Slow progressive muscle weakness occurring in individuals with a confirmed hx of acute polio
Attacks cell bodies of motor neurons
20-40 years after initial attack (30-40%)
Common impairments
Fatigue
Pain
Muscle weakness (asymmetrical)
Hypotonicity
reactivation of dorminal polovirus; large motor units overworked
PT intervention PS
Strengthening- be careful to avoid fatigue and muscle soreness
Aerobic capacity
Submax principles, low-mod intensity, frequent rest breaks
Whole body movements, focus on FUNCTION
Maintain respiratory function, energy conservation
Orthotics, DME
Research lacking
moderate resistance with near normal strength - avoid muscle training with severe paresis
NMJ disorders - Myasthenis Gravis
Postsynaptic neuromuscular junction disorder characterized by progressive muscle weakness and fatigability with exertion
Autoimmune antibody-mediated attack on acetylcholine receptors and NMJ
Acetylcholine receptors are destroyed
Prevents muscles from contracting
Course varies (may progress from mild to severe)
MG Signs and Symptoms
Fatigue or weakness with sustained activity
Muscular strength worse with continuing contraction, improved with rest
Four types
Ocular myasthenia (confined to extraocular muscles)
Mild generalized myasthenia
Severe generalized myasthenia
Crisis
MG with respiratory failure = medical emergency!!
PT exam MG
Cranial nerves (diplopia, ptosis, dysarthria, dysphagia, facial expression)
Ice pack test- positive test is decreased ptosis after 2 min application of an ice pack to affected eyelid
Muscle strength- proximal muscles more involved than distal
Fatigability- repeated muscle use results in rapid weakness
Functional mobility
medical Dx MG
neuro exam
blood test (elevated antibodies) EMG/NCV, CT/MRI
Most people with myasthenia gravis have elevated levels of antibodies that attack acetylcholine receptor sites in the neuromuscular junction and prevent muscles from contracting.
ice pack screening*
PT treatment: MG
Patient/family education
Safe functional mobility
Energy conservation techniques
Respiratory training
Muscle strengthening (2-3x/wk)
Include respiratory exercises
Moderate intensity (low with fatigue)
Focus on large, proximal muscle groups
Weight bearing activities
Balance training (1-2x/wk)
Aerobic exercise (low intensity: 30-50% VO2)
OT/SLP referral
PA and MG
No side effects have been linked to physical training in individuals with MG. However, it is suggested to restrict it to patients with mild to moderate symptomatology (stage IIA and IIB of the disease)
Evidence indicates that moderate intensity aerobic- and strength exercise is advantageous for patients with muscle diseases, without causing harmful exercise-induced muscle damage.
On the contrary, motor neuron diseases show a rather blunted response from exercise training. High-intensity training is a modality that seems safe and a promising exercise method, which may circumvent neural fatigue and provide effect to patients with motor neuron disease.
Although we have come far in changing the view on exercise therapy in neuromuscular diseases to a positive one, much knowledge is still needed on what dose of time, intensity and duration should be implemented for different diseases and how to provide exercise therapy to very weak, non-ambulatory and wheelchair bound patients.
