Guillan Barre Syndrome Flashcards
Guiilanne Barre Syndrome Pathology
Immune-Mediated Polyneurpathy
Resulting from a preceding infection that reacts with the ANS and produces inflammation in the peripheral nerve
Where is Guillain Barre Syndrome directed?
Directed toward the Nerve Root
Leading to a Motor and Sensory Neuropathy
Most common and severe Paralytic Neuropathy
3 Types of Gullian-Barre
Acute Motor Axonal Neuropathy (AMAN)
Acute-Motor Sensory Axonal Neuropathy (AMSAM)
Miller-Fischer Syndrome
Acute Motor Axonal Neuropathy (AMAN)
Axons (Nerve Fibers) rather than Myelin Sheath
Arm and Leg involvement
Acute Motor-Sensory Axonal Neuropathy (AMSAN)
Combination of Myelin and Axons damage
Miller-Fischer Syndrome
Rare Variant
Weakness or paralysis of the Eye Muscles
Epidemiology of Guillain Barre
Incidence: 1-2/100,000 per year)
Increases by ~20% with every decade of life beyond the first 10 years of age
Greater in MALES than females
Children 0-18 years
Guillain Barre: Autoimmune Disease
ACUTE demyelinating process of the peripheral nerves
Cell mediated PN disruption (Immune Cell Mediated)
Secondary Hypersensitivity Reaction
Elevated Cytokines in CSF, PN, Serum
Guillain Barre: Pathogenesis
2/3rds associated with bacterial or viral origin (2 wks prior)
Moves through the GI or Respiratory System
(Mucosal or Epithelium)
Guillain Syndrome Subtypes
(Demyelinating)
Acute Inflammatory Demyelinating Polyneuropathy
(Axonal)
Acute Motor Axonal Neuropathy
Guillain Syndrome Subtypes:
(Demyelinating)
Anti body injures myelin membranes
Guillain Syndrome Subtypes:
(Axonal)
Antibody injures Axonal Membranes
Pathogenesis of Guillain Barre (EXAM)
Infiltration of macrophages and T lymphocytes into the Spinal Roots and PN
Macrophages attack and strip the myelin
(Mild Cases = Axons intact)
(Severe Cases = Axons Destroyed)
Saltatory Conduction is reduced or disrupted
Varies from partial to complete
Guillain Barre Pathogens
Respiratory or diarrhea prior to illness (2-3 weeks)
Campylobacter Jejuni infection is most common
(Bacterial Gastroenteritis)
Cytomegalovirus, Epstein-Barr virus, and Human Immunodeficiency Virus (HIV) infection
A small % of patients develop GBS after another triggering event such as immunization, surgery, trauma, and bone-marrow transplantation
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
Similar clinical presentation to GBS
Slow progression up to 8 weeks
Persists for years (Chronic)
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
Does not involve the respiratory system
Rarely precluded by infection
Relapses are much more frequent
Longer recovery time
Corticosteroids effective
Clinical Presentation GBS:
Evolution
Acute (hours) or slowly over 3-4 weeks
Clinical Presentation of GBS:
Symptoms
Symmetrical ascending weakness from distal LEs to UE / Respiratory Systems
Varies from mild distal to total paralysis / intubation
Accompanied by severe fatigue
20-38% are intubated from intercostal and diaphragmatic weakness
Guillain Barre:
Clinical Presentation 1st Symptoms
Symmetrical
Numbness and Tingling
Ascending Muscular Weakness Distal to Proximal
Guillain Barre:
Clinical Presentation Areflexia
Ascending Loss and hypotonia
Guillain Barre:
Clinical Presentation Autonomic Symptoms
50% of persons
Tachycardia
Low Cardiac Output: Hypotension (Postural)
Cardiac Arrhythmias (20%)
Hypertension: BP Dysregulation
Peripheral pooling of blood
Urinary retention
Guillain Barre:
Clinical Presentation
Sensory Loss and Pain
Guillain Barre: Clinical Presentation of Sensory Loss
Vibration or Position Sense
Paresthesias
Stocking and Glove Pattern
Guillain Barre:
Clinical Presentation of Pain
Prominent: Muscular Aching associated with activity (stretching)
Severe burning or hypersensitivity
(Demyelination)
PROM: proximal Muscle groups
Sensory Nerve regrowth from WB & Ex