GBS
GBS
GBS
Pathogenesis
Acute autoimmune
disorder
There is involvement
of T lymphocytes and
B lymphocytes
Brain is unable to send
messages
Legs and arms are
commonly affected
Etiology
Etiology
Clinical Manifestations
Signs and Symptoms Include
Paresthesia
Muscle Weakness
Possible Paralysis
Clinical Manifestations
Rapidly evolving (hours to days)
Areflexic motor paralysis: Rubbery legs
Sensory loss Proprioception
Usually upward progressing
Lower cranial nerves: OP dysphagia
Pain: Deep aching pain
Transient bladder dysfunction
Antecedent Events
70% of cases occur 1-3 weeks after infectious
process
20-30% of all cases are associated with
Campylobacter jejuni (summer outbreaks in
China among kids and young adults)
Also HHV, CMV or EBV
Mycoplasma pneumoniae
Recent Immunizations
Lymphoma (Hodgkins)
HIV
SLE
Molecular Mimicry
Immune responses to non-self antigens
Misdirect to host nerve tissue through resemblance
Neural targets are gangliosides, particularly at the
Nodes of Ranvier
Molecular Mimicry
Diagnosis
Rapid development of muscle paralysis,
Differential Diagnosis
Acute Myelopathies
Botulism
Diptheria
Lyme disease with polyradiculitis
Porphyria
Vasculitis Neuropathy
Poliomyelitis
CMV polyradiculitis
Critical Illness Neuropathy
Myasthenia Gravis
Poisonings with Organophosphates or arsenic
Paresis from West Nile Virus
Spinal Astrocytoma
Motor Neuron Disease
Treatment
There is no cure for Guillain-Barr Syndrome, but
there are treatments available
Plasmapharesis
Immunoglobulins
Treatment
Supportive Management: Telemetry, Blood
Prognosis
Most of the time recovery starts after the 4 th