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Pathophysiology II > Guillain-Barre Syndrome > Flashcards

Guillain-Barre Syndrome Flashcards

1
Q

What is GBS?

A

Most common cause of rapidly evolving motor paresis and paralysis and sensory deficits

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2
Q

What is the incidence? M vs F? Mortality?

A
  1. Incidence is 1-2 cases per 100,000 people
  2. Affects all ages (esp. young adults and individuals between 50-80 yrs)
  3. M>F
  4. Mortality > 5%
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3
Q

GBS is a syndrome. What 4 conditions does it include?

A
  1. Flaccid Paralysis
  2. Areflexia
  3. Respiratory Compromise
  4. Autonomic Dysfunction
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4
Q

What are the characteristics of flaccid paralysis?

A
  1. Maximal weakness ~2-3 weeks after onset
  2. Facial weakness >50% of cases
  3. Pharyngeal weakness
  4. Laryngeal weakness
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5
Q

Pharyngeal and laryngeal weakness can lead to ______.

A

ASPIRATION

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6
Q

Mechanical ventilation is needed in ____% of cases

A

25-30%

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7
Q

Autonomic dysreflexia occurs in _____% of cases. Characteristics?

A

70%

  1. Fluctuations in heart rate, rhythm, and BP
  2. Excessive or loss of sweating
  3. Flushing of face
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8
Q

What is the etiology of GBS?

A

Autoimmune disorder –> antibody mediated demyelination

Myelin sheath on peripheral nerves is attacked causing demyelination (Classic type of GBS)

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9
Q

______ cells are spared allowing for future recovery and re-myelination.

A

SCHWANN CELLS

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10
Q

60-90% of patients with GBS report experiencing ____ 30 days before onset of GBS.

A

INFECTION (minor illness)

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11
Q

How long does it take for the body to initiate its healing processes following the onset of GBS?

A

~ 2 to 4 weeks

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12
Q

What is the onset of GBS like? When does it peak?

A
  1. Onset and progression are fast
  2. 50% of cases peak in 2 weeks
  3. 90% of cases peak in 4 weeks
  4. 10% recur
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13
Q

What are the clinical signs and symptoms of GBS?

A
  1. “Stocking Glove” presentation at first
  2. Begins with paraesthesias in toes / fingers and distal leg weakness / hand weakness
  3. Weakness and paraesthesias progress proximally including trunk
    Face and palate in ~50% of cases
  4. Respiratory paralysis requiring mechanical ventilation in ~ 25-30% of cases within ~ 18 days
  5. May cause total paralysis/dysphagia
  6. Bowel and bladder dysfunction are rare
  7. Fever is not typical
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14
Q

What are possible differential diagnoses for GBS?

A 
Hysteria
Tick paralysis 
Toxic neuropathy
Myasthenia gravis
Neuromuscular blocking agents
Transverse myelitis
Anterior spinal artery syndrome
Poliomyelitis
Stroke
Metabolic disorders
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15
Q

How is GBS diagnosed?

A

Basic lab studies ordered to r/o other pathologies

Albuminocytologic Dissociation is present
(Increased protein in the cerebrospinal fluid without increase in white blood cell count = widespread inflammation of nerve roots)

  1. Nerve conduction studies to detect demyelination
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16
Q

What diagnostic criteria must be met to establish a diagnosis of GBS?

A
  1. Progressive, symmetric weakness in more than one extremity
  2. Sensory deficits
  3. Loss of deep tendon reflexes
  4. Possible tachycardia, cardiac arrhythmias, labile blood pressures
  5. Absence of fever
  6. Electrophysiological tests reveal signs of demyelination
  7. Cerebral spinal fluid analysis via lumbar puncture 1 week post-onset of symptoms reveals
    increased protein (albumin) and <10 WBC’s and lymphocytes
17
Q

Plasmapheresis is used to manage GBS. What is it? What are 2 benefits associated with plasmapheresis?

A
  1. The process of removing plasma from the circulatory system and filtering it in order to remove antibodies
  2. Plasma is then returned to the circulatory system
  3. Performed 4-6 x over period of 1 week
  4. Shown to reduce time on respirator
  5. Shown to reduce time to independent ambulation

***Intravenous Immunoglobulins (IV Ig) also used to manage GBS

18
Q

_______ do not have any beneficial effect in classic GBS

A

Corticosteroids

19
Q

The period between peak impairment and recovery is called the ______ phase.

A

Plateau or static phase

20
Q

How does recovery from GBS typically progress ?

A

Proximal to distal (opposite to the onset)

21
Q

How long does it take to recover from GBS?

A
  1. May take weeks to years for recovery
  2. One year post onset, 67% of people have full recovery
  3. Up to 20% have lasting neurological impairments
  4. After 2 years, up to 8% have not recovered
22
Q

What are 5 poor prognostic indicators of GBS?

A
  1. Advanced age at onset
  2. Protracted time between peak impairment and onset of recovery
  3. Need for mechanical ventilation
  4. Evidence of axonal degeneration (reduced evoked motor potential)
  5. Cranial nerve involvement
23
Q

What are 5 good prognostic indicators of GBS?

A
  1. Younger age at onset
  2. Less time between peak impairment and onset of recovery
  3. Less total impairment
  4. No need for mechanical ventilation
  5. Intact axonal integrity
24
Q

What are 6 variants of GBS?

A
  1. Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) –> classic form
  2. Acute Motor Axonal Neuropathy (AMAN)
  3. Acute Sensory Ascending Neuropathy (ASAN)
  4. Acute Motor and Sensory Axonal Neuropathy (AMSAN)
  5. Miller Fisher Syndrome
  6. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
25
Q

What is Acute Motor Axonal Neuropathy (AMAN)?

A
  1. Most severe variant of GBS
  2. Often follows episode of diarrhea
  3. Frequent respiratory involvement and ventilator dependence
  4. Does not affect sensory nerves
  5. Significant residual impairments
26
Q

What is Acute Sensory Ascending Neuropathy (ASAN)?

A

Sensory changes more prominent than weakness

27
Q

What is Acute Motor and Sensory Axonal Neuropathy (AMSAN)?

A
  1. Acute Autonomic Neuropathy
  2. Postural hypotension
  3. Impaired sweating
  4. Impaired bowel and bladder function
28
Q

What is Miller Fisher Syndrome?

A
  1. Abnormal muscle coordination and ataxia
  2. Paralysis of eye muscles results in diplopia and sluggish pupillary light reflexes
  3. Facial weakness
  4. Absence of DTRs
  5. A unique antibody is characteristic to differentiate from other forms of GBS
29
Q

What are the symptoms of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)? Progression? M vs F?

A
  1. Signs/Symptoms are similar to classic type of GBS, but may be more diffuse
  2. Progression of disease is slower than classic GBS ( > 8 weeks up to a year)
  3. F>M
  4. More common in younger adults
  5. Neuropathic pain
30
Q

How is Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) diagnosed?

A
  1. Because of slow, long onset, diagnosis may be delayed
  2. Lack of treatment may lead to severe nerve damage that may not recover
  3. Requires nerve biopsy in most cases
31
Q

How is Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) treated?

A
  1. Corticosteroids alone or in combination with immunosuppressant drugs
  2. Plasmapheresis
  3. IV Immunoglobulin
  4. Ventilatory support as needed
  5. Physical Therapy
32
Q

What are 5 long term complications of steroids?

A
  1. Behavioral: mood swings, insomnia
  2. Fluid retention, increased BP, glaucoma
  3. Weight gain with fat deposits in abdomen, face, and posterior neck
  4. Fractures, osteoporosis, bruising
  5. Increased risk of infection
33
Q

What is the prognosis for Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)?

A
  1. May have one bout and then spontaneous recovery
  2. May have several recurrences with partial recovery in between over the course of years
  3. May progressively worsen without improvement
34
Q

TRUE or FALSE: Functional electrical neuromuscular stimulation (FES/NMES) is useful due to demyelination

A

FALSE

FES/NMES is not useful for demyelination

35
Q

What should be avoided when exercising patients with GBS?

A

Avoid over-exercising diseased muscle units

May result in further motor unit damage
May result in central fatigue and chronic fatigue

Pathophysiology II (24 decks)

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