Acute inflammatory demyelinating polyradiculoneuropathy Guillain-Barre Syndrome Medicine Physiotherapy

Diagnosis of Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome)

In this article we will discuss the diagnosis of acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome)

In this article we will discuss the Diagnosis of acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome). So let’s get started.


The cerebrospinal fluid examination and cereal electrophysiological studies are critical for confirming the diagnosis of Guillain-Barre syndrome other tests are inconsequential.

1. CSF examination: Initially in GBS, the CSF may be normal, then becomes abnormal within 3 to 5 days on subsequent examinations and shows elevated proteins (800 to 1000 mg/dl) with normal cell count (albuminocytological dissociation). If the CSF cell count is greater than 20 mononuclear cells/m3, one should think of HIV infection, viral transverse myelitis, leukemia, lymphoma, neurosarcoidosis. Transient oligoclonal IgG bands and elevated myelin basic protein levels may be detected in CSF in some patients in approximately 10% of patients CSF proteins may remain normal throughout the period of Guillain-Barre syndrome.

2. Electrophysiological studies: Abnormalities on electrophysiological studies have been documented in about 90% cases of Guillain-Barre syndrome and reflect multifocal demyelination associated with secondary axonal degeneration. The electrophysiological studies i.e. nerve conduction may reveal increased distal latency, conduction slowing, conductions block; F wave slowing and decreased nerve conduction velocities. The electromyography shows decreased motor unit recruitment. Subsequently, if any amount of axonal degeneration occurs, or AMAN or AMSAN develops, then there is reduced amplitude of motor action potentials, fibrillation potentials appear 2 to 4 weeks after the onset.

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