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Neuro II > Guillain-Barré Syndrome > Flashcards

Guillain-Barré Syndrome Flashcards

General characteristics, background, clinical presentation, diagnosis, clinical variants, clinical course and potential complications, identify prognostic considerations, outcome measures, CIDP

1
Q

What is the pathophysiology behind GBS?

A

Immune system attacks Schwann cells in PNS

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2
Q

What populations does this diagnosis
demonstrate incidence trends towards?

A
  • Young adults, 50-80s (*Highest in those >60, 20% increase for every 10-year increase in age)
  • MALES > females
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3
Q

Describe the etiology of GBS.

A
  • Idiopathic vs viral/bacteria
  • Autoimmune
  • Allergic response
  • HIV/herpes
  • Vaccinations
  • Surgery/trauma
  • Post-partum
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4
Q

Bacterial etiology of GBS is often associated with:
- Epstein Barr
- Upper respiratory infections
- GI infections
- Undercooked food

A

Undercooked food

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5
Q

T/F viral etiologies of GBS co-incide (simultaneous occurance) with GBS symptoms

A

False, virual infection preceeds GBS by 1-4 weeks

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6
Q

Explain the typical clinical presentation of GBS.

A

Initially rapid progression of symptoms distal to proximal, 12-28 hours > plateau (“nadir”) for 2-4 weeks > gradual recovery proximal to distal

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7
Q

What are common signs and symptoms associated with this diagnosis?

A
  • Weakness (rapid, progressive, symmetrical, distal to proximal, LE before UE 90% of time)
  • Hyporeflexia/areflexia
  • Hypotonia
  • Facciculations
  • CN involvement: CN VII, CN III, IV, VI, CN IX, X
  • PAIN
  • Autonomic dysfunction
  • Respiratory difficulties
  • Sensory symptoms (late)
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8
Q

How is GBS diagnosed?

A
  • CSF Examination: increased protein levels
  • NCV:
    • reduced amplitude/absent distal motor AP
      - ↓ conduction velocity
      - ↑ temporal dispersion
      - Latency prolongation of F-wave
      - Nerve conduction block (axonal GBS)
  • MRI (RO): enhancement/swelling of spinal n. root
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9
Q

Required Featuers of GBS:

NINDS Criteria

A
  • Progressive, symmetrical weakness of LE + UE (minimal to total paralysis)
  • Areflexia/hyporeflexia
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10
Q

Supportive Features of GBS

NINDS Criteria

A
  • Progression of symptoms <4 weeks (80% reach nadir in 2 wks)
  • Relative symmetry
  • Mild sensory S&S
  • Cranial nerve involvement (esp bilateral facial n. weakness)
  • Recovery starts 2-4 weeks after progression halts
  • Autonomic dysfunction
  • Pain
  • No fever at onset
  • Elevated protein in CSF
  • Electrodiagnostic abnormalities consistent with GBS
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11
Q

Doubtful Features of GBS Dx

NINDS Criteria

A
  • Sensory > motor loss
  • Marked, persistent asymmetry of weakness
  • Bowel and bladder dysfunction at onset (or persistent)
  • Severe pulmonary dysfunction with little to no limb weakness at onset
  • Fever at onset
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12
Q

Which GBS clinical variant am I?

  • Progressive, symmetrical muscle weakness, absent or depressed DTRs
  • Often with preceding illness
A

Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP)

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13
Q

Which GBS clinical variant am I?

  • Ophthalmoplegia
  • Ataxia
  • Areflexia
    (Especially of face)
  • 25% develop extremity weakness
A

Miller-Fisher Syndrome

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14
Q

Which GBS clinical variant am I?

  • Axonal involvement
  • Muscle weakness
  • Occasional preservation of DTRs
  • Sensory spared.
A

Acute Motor Axonal Neuropathy

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15
Q

Which GBS clinical variant am I?

  • Axonal involvement
  • Motor + sensory impacted
A

Acute Motor-Sensory Axonal Neuropathy

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16
Q

What is the goal of medical management of GBS?

A

Control the inflammatory response

17
Q

What are the major interventions for GBS in the acute setting?

A

IV Immunoglobulin (IVIg)
Plasma Exchange

18
Q

How does Intravenous Immunoglobulin (IVIg) work?

A

Plasma products made of antibodies extracted from blood given to patient. Thought to block macrophage/antibody binding.

19
Q

How does Plasma exchange (plasmapheresis) work?

A

Blood removed and separated into plasma and cells - cells transferred back into bloodstream.

Typical treatment 5 exchanges/2-week period

20
Q

When is plasma exchange reccommended?

A

If a pt is unable to walk 10 meters w/o assistance

21
Q

What are the benefits of Intravenous Immunoglobulin (IVIg)?

A
  • Thought to prevent myelin loss and axonal damage = significant improvements
  • Aid in sustained remission
22
Q

What are the benefits of Plasma exchange (plasmapheresis)?

A
  • Reduced n. damage
  • faster clinical improvement
23
Q

Describe the Acute Phase of the clinical course of GBS

A
  • Rapid progression of symptoms that peak after 2-4 weeks
  • 50% reach max impairment w/in 1 week.
  • 70% reach max impairment w/in 2 weeks.
  • 80% reach max impairment w/in 3 weeks.
  • 98% reach max impairment w/in 4 weeks.
24
Q

Describe the Plateau Phase of the clinical course of GBS

A
  • Stability of symptoms
  • Days - 1 Month
25
Q

Describe the Recovery Phase of the clinical course of GBS

A
  • Gradual improvement in symptoms (indv. time frame)
  • Most 2-4 weeks after plateau
  • Sensory disturbance and fatigue can persist for years
26
Q

What are some potential complications in the acute phases of GBS?

A
  • Respiratory impairment and failure
  • Autonomic instability
  • Pain
  • Pneumonia
  • Prolonged hospitalization and immobility (DVT, skin breakdown, contracture)
  • Relapse if treatment inadequate
27
Q

Which of the following is true regarding total recovery time from GBS:
a. Increased risk of relapses with subsequent infections.
b. Moderate to severe sensory impairments are common
c. 20% of patients experience persistent disability
d. 80% recover previous level of ambulation status by 6 month

A

c. 20% of patients experience persistent disability

28
Q

What are common lingering symptoms with GBS?

A
  • Paresthesias, distal muscle weakness (foot drop)
  • Mod - severe pain
  • Extreme fatigue (67% of patients)
  • Minor neurological deficits
  • 2% progress to CIDP
29
Q

What factors increase the risk of long term morbidity and mortality?

A
  • Prolonged course with months of ventilatory support/incomplete recovery
  • Pulmonary/cardiac complications
  • Organ failure
30
Q

What does the EGRIS seek to determine?

A

Risk of developing respiratory failure in 1st week of admission.

31
Q

Negative Prognostic Indicators for GBS

A
  • Older age at onset (>60)
  • Need for ventilatory support
  • Rapid onset (<7 days) prior to admission
  • Avg. distal motor response amplitude reduction on electrodiagnostic testing to <20% normal
  • Hx of GI illness prior to onset (presence of diarrhea)
32
Q

What patient characteristics does the EGRIS include in it’s assessment?

A
  • Days between onset of weakness and hospital admission
  • Facial or bulbar weakness at time of admission
  • UE/LE strength at time of admission

1 in 3 pt’s requires ventilatory support!!

33
Q

What does the EGOS seek to determine?

A

ability to walk at 6 months

34
Q

What patient characteristics does the EGOS include in it’s assessment?

A
  • Age at onset
  • Preceding diarrhea in last 4 weeks
  • Modified (1 week): UE/LE strength at day 7 of admission
  • Original (2 week): GBS disability score at 2 weeks after hospital admission
35
Q

What does the GBS Distability Scale Measure?

A

Global Disability (health to death, mobility status, assisted vent)

36
Q

What does the Overall Disability Sum Score assess?

A
  • UE/LE functional tasks (no to severe disability score)
  • Significant association with patient’s own perception of clinical condition
37
Q

How does Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) differ from GBS?

A
  • Unknown etiology
  • Chronic
  • Gradual onset
    • > 8 weeks from onset before plateau signs
    • Motor AND sensory involvement
    • Symmetric or asymmetric
  • No improvement after plateau occurs
  • Onion bulb changes
  • Responds to glucocorticoids (minimal)

Neuro II (17 decks)

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