Guillain Barre Syndrome

Mortality ranges from 2%-12%, 15% have persistent disability.

The lifetime risk is estimated at one in 1000.

The incidence increases with age, and males are slightly more likely to develop GBS than females.

An acute inflammatory demyelinating polyradiculoneuropathy.

A peripheral neuropathy of acute onset characterized by rapidly developing motor weakness and areflexia.

An auto immune disease that affects the peripheral nervous system and develops over several days to weeks.

An autoimmune disease triggered by stimulus of external origin.

An immune mediated illness manifested as progressive paralysis over 1 to 3 weeks, with a 5% death rate and up to 20% of patients left with significant disabilities.

The most common subtypes are acute inflammatory demyelinating polyradiculoneuropathy and acute motor axonal neuropathy.

Approximately 90% of people with GBS in North America and Europe have acute inflammatory demyelinating polyradiculoneuropathy.

Approximately 2/3 of patients have a diarrheal or respiratory illness within 4 to 6 weeks prior to the onset of GBS symptoms.

Associated with a small but significant risk following administration of influenza vaccines.

May be triggered by recent surgery, pregnancy, and immuno suppression?

Associated with Zika virus, Japanese encephalitis virus, West Nile virus dengue viruses, and live attenuated yellow fever vaccine.

20%-30% require mechanical ventilation and of those 15%-30% die.

40-70% of mechanical ventilated patients develop evidence of pneumonia.

An acute autoimmune neuropathy affecting motor function manifested by progressive, symmetrical, ascending weakness associated with paresthesias and decreased or absent muscle stretch reflexes.

Cranial nerve involvement can cause facial muscle weakness, nasal speech and dysphagia.

In more than 50% of cases, cranial nerves originating in the brainstem are affected, causing facial weakness, difficulty swallowing, and eye muscle weakness or paralysis.

Majority of episodes begin 5 days to 3 weeks after a febrile illness, a diarrheal disease, immunization, or surgery.

Majority of cases are monophasic with most impairment by four weeks and most patients manifesting full recovery as long as 24 months later.

Weakness often ascending, but arms and face may be affected first.

Oropharyngeal weakness can develop, as can diaphragmatic weakness.

About 25 to 30% of patients develop severe weakness or paralysis of the muscles used to breathe.

GBS commonly causes low back pain and limb, numbness and tingling, and fluctuations in blood pressure or an irregular heart rhythm.

Central fat is associated with cardiometabolic risk factors in young individuals.

Rarely presents with bilateral facial palsy.

CSF is most often acellular.

CSF protein level is typically highly elevated.

Neuroimaging is most often normal or shows only subtle enhancement of nerve roots.

Diagnosis is based on symptoms and physical examination findings.

Neurological testing, including electromyography and nerve conduction studies assess nerve and muscle function.

Lumbar puncture findings can support the diagnosis and can rule out of the neurological diseases.

Standard of care is to use IV IgG or plasma exchange for patients who do not have independent ambulation within 2 weeks of onset of the disease.

About 40 to 50% of patients with GBS do not improve within four weeks after IVIG or plasma exchange and need prolonged supportive care.


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