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Neuro Rehab 2 > GBS > Flashcards

GBS Flashcards

1
Q

what is GBS

A

most common form of autoimmune inflammatory demyelinating polyradiculoneuropathies

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2
Q

what is the etiology of 75% of GBS cases

A

preceded by acute infection 2wks prior
- URI, campylobacter jejuni, epstein barr, mycoplasma pneumonia, cytomegalovirus
- vax
- strong association w zika virus

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3
Q

what is the pathophys of GBS

A

auto-immune attack on schwann cells of peripheral nerves:

antigens trigger mobilization of macrophages and lymphocytes -> migration to nodes of ranvier, attack schwann cells and strip myelin away -> slow conduction velocity
- axon may degen

progressive demyelination phase limited to 4wks**
- remyelination usually begins w/i 2-3wks as long as axons are good and haven’t died off

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4
Q

what is the typical age of onset

A

30s-50s
- can occur anywhere in the lifespan

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5
Q

is there any geographic clustering of GBS

A

no - except for recent cases w Zika virus outbreaks

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6
Q

what are 4 methods of dx

A

lumbar puncture
EMG
NCV
presence of clinical features w course <4wks

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7
Q

how can a lumbar puncture dx GBS

A

presence of excess protein in CSF d/t demyelination but no inc in WBCs

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8
Q

if clinical features of GBS last >4wks, what does this indicate

A

different health condition than GBS
- CIDP likely

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9
Q

how can an EMG dx GBS and what is a limitation

A

(+) for fibrillation potentials
- as axon degen, leads to loss of innervation and can see fibrillation

if mild case, may be w/i normal limits

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10
Q

how can a NCV dx GBS

A

shows slow nerve conduction velocity and/or conduction block
- myelin is what inc conduction speed to jump b/w nodes

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11
Q

what are clinical sx present for <4wks that may dx GBS

A

progressive, relatively symmetrical weakness w areflexia and exclusion of other causes
- starts distal -> prox
- recovery starts prox -> distal

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12
Q

what are 6 differential dx for GBS

A

CIDP
lyme dz/tick paralysis
MG
neuropathy
cord compression/cauda equine syndrome
FND

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13
Q

how do you distinguish CIDP from GBS

A

chronic inflammatory demyelinating polyneuropathy sx last >4wks

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14
Q

how do you distinguish lyme dz or tick paralysis from GBS

A

biomarkers to indicate lyme dz

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15
Q

how do you distinguish myasthenia gravis (MG) from GBS

A

path of MG is in NMJ
- pattern of onset is different

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16
Q

how do you distinguish a neuropathy from GBS

A

causes of neuropathy like HIV, DM, ETOH, toxic, metabolic

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17
Q

how do you distinguish FND from GBS

A

similar onset of weakness (symmetrical), but not attributed to any path as FND is psychosomatic/genic in nature

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18
Q

what is nadir

A

when sx reach maximal severity and plateau and stabilize
- once reach nadir, go into recovery phase

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19
Q

what is the prognosis for GBS

A

most reach nadir w/i 1wk
most regain amb function

1/2 have minor residual deficits (ie dec DTR and strength)

few have permanent severe disability or develop CIDP

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20
Q

what can contribute to different prognoses in GBS

A

remyelination starts at cell body of axons
- shorter nerves innervating prox ms regain function sooner
- longer axons in peripheral ms take longer

if axon degen/dies off

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21
Q

what are reasons for a permanent severe disability prognosis

A

axons degen/die off - recovery from axon sprouting or nearby axon reinnervating
- limited

dec amb d/t pretibial ms weakness

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22
Q

what are reasons for mortality in GBS

A

respiratory failure
cardiac issues
organ failure

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23
Q

what are 6 poor prognostic indicators

A

need for vent support
CN involvement (ie swallowing)
axonal damage
advanced age
preceding GI or CMV infection
rapid progress to quad w/i 1wk of onset

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24
Q

what are 5 clinical features of GBS

A
  1. rapid progression of symmetrical weakness or varying severity
  2. diminished or absent DTRs
  3. joint pain & myalgia
  4. stocking & glove pattern of sensory disturbances
  5. autonomic dysregulation
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25
Q

when does recovery typically begin

A

2-4wks after plateau

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26
Q

what are 3 motor sx of GBS

A
  1. progressive rapid development of weakness
    - limbs, face, eyes, trunk, and/or oropharyngeal ms
  2. (B) symmetrical distal->prox
  3. mild to total paralysis/quadriplegia w respiratory and CN involvement
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27
Q

what are 5 characteristics of sensory disturbances often seen in GBS

A
  1. typically before ms weakness
  2. distal-> prox loss in “stocking glove” pattern
  3. return occurs prox to distal pattern
  4. hyperesthesia, paresthesias
  5. dec vibratory sense and proprioception
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28
Q

what is hyperesthesia and why is this seen in GBS

A

every sensory input is perceived as pain
- super difficult to manage

axons that carry pain, pressure, light touch are demyelinated
pain from C fibers don’t have myelin and are the only nerves that aren’t really impacted

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29
Q

what are 5 qualities of pain in GBS

A
  1. associated w pressure areas and lengthening/stretching long, myelinated axons
  2. worse at night
  3. aching, burning, radicular pain
  4. symmetrical, often in large ms groups (ie gluts, quads, hamstrings)
  5. soft tissue stiffness at late stage contributes to pain
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30
Q

what are qualities of autonomic dysfunction seen in GBS

A

cardiac arrhythmias **
dec cardiac outputs, abnormal EKG, BP fluctuations, sweating abnormalities (problems w thermoregulation), pupillary dysfunction

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31
Q

why do more than 50% have OH as autonomic dysfunction clinical feature

A

likely d/t dec ms tone in LEs
- no ms contraction/tone to get venous return to maintain BP

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32
Q

if someone w suspected GBS has intact reflexes what does this indicate

A

suggestive of an alternative dx
- 70% of people w GBS have dec or absent reflexes

33
Q

what cranial nerve involvement can be seen in GBS

A

facial weakness
opthalmoparesis
- eye mvmts
oropharyngeal weakness
- difficulty speaking, swallowing

34
Q

what are the 2 gold standards for treatment of GBS and how would you choose b/w them

A

plasmaphoresis
IV immunoglobulin

same benefit, IVIg is less invasive

35
Q

plasmaphoresis: how does it work, when is it most effective, and benefits

A

5-10day course of treatment removing immunoglobulins and cytokines and replacing them w albumin (a neutral protein) via a large catheter in arm

w/i 1wk of sx for optimal effect
- can benefit pts up to 30 days after dx (tho likely not same effect on recovery)

shortens recovery time by 1/2 for (I) respiratory function and return to amb

36
Q

IV immunoglobulin: how does it work, and benefits

A

5 daily infusions that neutralize autoantibodies and dec level of inflammatory cytokines
- dilutes concentration of immune cells in bloodstream thus dec impact of inflammatory cells

dec recovery time by 1/2 if initiated early in dz process

37
Q

what are 5 components of medical management outside of the gold standard treatments

A

corticosteroids
vent support/pulm hygiene
autonomic dysregulation
pain meds
DVT/PE prophylaxis

38
Q

what does evidence say about the use of corticosteroids

A

lacks evidence, but still widely prescribed

39
Q

what medical management might autonomic dysregulation need

A

may need meds for transient HTN or HoTN
pacer for severe bradycardia or tachycardia (less common)

40
Q

why are pain meds prescribed and what does evidence say

A

neuropathic pain and hyperesthesia common

poor response to most pain meds

41
Q

why do we want to do aggressive DVT/PE prophylaxis

A

high risk d/t weakness

42
Q

what are 3 examples of DVT/PE prophylaxis

A

heparin
compression stockings
PROM -> A/AROM

43
Q

what are 6 interventions in the progressive phase of the dz

A

supportive care
promote pulm hygiene
skin protection
pain management
OH mgmt & monitor VS
psychosocial support

44
Q

how can ROM be used to manage pain

A

w widely distributed force w open hands and cradle w arms
- may inc pain in short term but dec pain (ms aching, cramping, and discomfort) after

45
Q

how can TENS be used for pain management

A

jam signals from C fibers to be transmitted to SC and perceived in sensory cortex

46
Q

how can ice packs be used for pain management

A

slow nerve conduction velocity, slow C fiber input and dec pain input

47
Q

how can ace wrapping be used for pain management

A

prolonged widespread contact tends to dec pain w other sensory inputs if person was then to move leg after

48
Q

what are examples of OH management options

A

abdominal corsets, anti-embolism stockings to maintain BP

49
Q

what are 5 interventions during the early recovery phase

A
  1. pulm hygiene, respiratory ms training
  2. pain management
  3. stretching
  4. prevention of secondary complications
  5. active ther-ex
50
Q

what must be avoided when doing interventions in the early recovery phase

A

avoid overuse damage
- can set back recovery

51
Q

what are parameters for stretching in the early recovery phase

A

gentle, avoid end-range for joint protection and pain management
- avoid traction on nerves that are recovering

52
Q

what are secondary complications to prevent in the early recovery phase

A

pressure ulcers
joint subluxations
disuse atrophy
respiratory infection
DVT

53
Q

what are parameters for active ther-ex in the early recovery phase

A

GM, A/AROM in ms 2/5 or less
- powder boards, no resistance
- few reps

54
Q

what is overuse damage in GBS and what is this d/t

A

prolonged weakness in the absolute strength and endurance of a ms d/t excessive activity

d/t repetitive recruitment of same motor units bc other motor units are unavailable

55
Q

what phase does overuse damage occur in

A

in early and/or late phase

56
Q

what are 3 sx of overuse damage

A

DOMS (1-5 days)
dec max isometric force
dec in function and strength

sx: ms aches, soreness, paresthesia

57
Q

what should a pt do if they recognize sx of overuse damage

A

rest until back to baseline

58
Q

how can muscle fatigue and overuse damage be avoided

A

low reps and resistance
frequent rests
monitor response to activity
rotate ms groups
non-fatiguing activity/exercise

aerobic training w mod intensity 60% target HR or RPE 13/20

59
Q

what education should you provide a pt w GBS on nerve regen

A

nothing you can do to make nerves regen faster
- no benefit to aggressive ther-ex programs

60
Q

what exercise is overuse damage and fatigue more commonly seen from

A

eccentric contractions

61
Q

when and how do you progress exercise in GBS

A

if pt improves or shows no decline after one week
- slow progression
- monitor 3-7days before

62
Q

what are 3 key PT interventions for during the recovery phase

A
  1. functional mobility training
  2. CV endurance training
  3. graduated strength training
63
Q

what is criteria to graduate strength training from the recovery phase

A

should have >2/5 strength before AG activity, otherwise keep GM

should have >3/5 strength before eccentric activity

activity pacing and precautions to prevent overwork damage

64
Q

CIDP vs GBS

A

similar pathophys and clinical sx

CIDP has a different course w slow progressive weakness, sensory loss, areflexia
- chronic

65
Q

what is required for a CIDP dx

A

at least 2 months progressive onset of sx

66
Q

what is the etiology of CIDP

A

unknown

cluster cases seen following tetanus and flu vax

67
Q

what are the gold standards for medical management of CIDP

A

IVIg, plasmapheresis, and prednisone (corticosteroids)

68
Q

what are alternative agents for CIDP medical management outside of the gold standards

A

similar treatments to GBS
- immune modulators that dampen immune response

ex: interferons, rituximab, methotrexate, other chemo

69
Q

what are the 3 course variants for CIDP

A

monophasic
relapsing
progressive

70
Q

what is the lifespan of someone w CIDP impacted and not impacted by

A

not by clinical course
by functional capabilities

71
Q

what is a monophasic course CIDP variant

A

one episode of deterioration for >4wks followed by sustained improvement

72
Q

what is a relapsing course CIDP variant

A

at least 2 separate deteriorations and at least one improvement b/w episodes

  • plateau and be okay for awhile and then deteriorate
73
Q

what is a progressive course CIDP variant

A

gradual deterioration w no episodes of improvement

74
Q

what CIDP course variant has the poorest prognosis

A

progressive

75
Q

what are 3 good prognostic indicators in CIDP

A

symmetrical sx
distal nerve abnormalities
favorable response to initial steroid treatment

76
Q

what is the general prognosis of CIDP

A

normal lifespan typically achieved
- long term disability rate of 13-20% –> more common in progressive variant

77
Q

PT in CIDP vs GBS

A

really similar w similar avoidance of fatigue and overuse

78
Q

what is the focus of PT in CIDP

A

functional training and aerobic conditioning

Neuro Rehab 2 (48 decks)

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