How does it happen
It's all about diagnosing
Are you gonna help me
GBS-verse
Guillain BS
100

Most common causative infection

Campylobacter jejuni, CMV, EBV

100

What is the main component for diagnosis ?

clinical

ascending weakness and non-length dependent sensory symptoms

100
First line of tx

 Either intravenous immunoglobulin (IVIG) or plasma exchange

100

 The most common form of GBS in North America and Europe

Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)

100

How do you pronounce Guillain-Barré?

ghee-yan bar-ray

200

What structures are damaged?

Nerve insulation (myelin) and sometimes even the covered conducting part of the nerve (axon) is damaged

200

CSF finding? we want THAT specific term

albuminocytologic dissociation

200

When is patient not indicated for hospitalization?

able to walk unaided for more than 5 m and who are stable

200

A severe variant of GBS that is more common in Asia, Central America, and South America 

Acute motor-sensory axonal neuropathy (AMSAN)

200

What vaccination led to increased GBS

In 1976, flu vaccination against the influenza A/H1N1 antigen led to a well-documented, increased incidence of cases of GBS

300

What type of antibodies are formed?

Ganglioside antibodies

300

When to do EMG?

electrodiagnostic studies should be undertaken at 10 to 14 days after symptom onset due to the time for Wallerian degeneration of sensory and motor nerve fibers

300

When is tx most beneficial?

within 7 days after disease onset

300

Acute brainstem dysfunction variant

Bickerstaff brainstem encephalitis

300

Percentage of patients dying of GBS

Less than 2% of people die from GBS

400

Miller-fisher antibody

anti-GQ1B

400

MRI findings

Enhancement of the nerve roots, indicating a breakdown of the blood-nerve barrier due to inflammation

400

What treatment is preferred for pediatrics

IVIG

400

Rarest known variant of GBS

Acute Panautonomic Neuropathy

400

In 1859, is credited with the first reported case of what later came to be known as the GBS.

Octave Landry

500

Where do Anti-GD1a antibodies bind ?

paranodal myelin, nodes of Ranvier, and neuromuscular junction

500

GBS nadir

4 weeks

500

IVIG adminitration

0.4 g/kg bodyweight per day for five consecutive days

500

Patients initially diagnosed with GBS who have three or more periods with clinical deterioration, or a new deterioration after 8 weeks from onset of weakness

Acute onset CIDP

500

Third author of GBS paper in 1916

André Strohl

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