Guillain Barré Syndrome (GBS)

Synonyms in a broader sense

  • Acute idiopathic polyradiculoneuritis
  • Polyneuritis
  • Landry-Guillain- Barré-Strohl syndrome
  • Polyradiculitis
  • Idiopathic polyradiculo- neuropathy
  • Kissing Mouth Landry Syndrome
  • GBS

Definition

Guillain-Barré syndrome is a neurological disorder based on the demyelination of nerve fibers. Around the age of 25 and around the age of 60 there are two disease peaks. Men are more frequently affected than women. The frequency of Guillain-Barré syndrome is 1-2/100. 000/year.

History

This form of the disease, which progresses rapidly within one to two days, with severe paralysis affecting the legs, arms, neck and respiratory muscles, was described as early as 1859 by Jean-Baptiste-Octave Landry de Thézillat (1826 – 1865). He wrote a report on ten patients with acute ascending paralysis. For this reason, Landry’s paralysis is still referred to today as the “Guillain-Barré Syndrome” in cases of particularly rapidly developing severe courses of the disease.

Ernst von Leyden (1832 – 1910), already differentiated in 1880 between the “acute and subacute multiple neuritis” as primary inflammatory diseases of the nerve processes and the primary spinal cord diseases, especially poliomyelitis. Guillain-Barré syndrome should actually be called Guillain-Barré-Strohl syndrome. In 1916, Georges Guillain, Jean Alexandre Barré and André Strohl were the first to describe the typically elevated protein level in normal cell numbers (cytoalbuminary dissociation) in the cerebrospinal fluid (liquor) of a patient suffering from acute radiculoneuritis (inflammation of the nerve roots), which is typical of Guillain-Barré syndrome.

The extraction of cerebrospinal fluid (liquor puncture) for so-called liquor diagnostics was invented in 1891 by the German internist Heinrich Irenaeus Quincke. The first larger-scale representation of the anatomical-pathological changes in Guillain-Barré syndromeGBS was compiled by W. Haymaker and J. W. Kernohan. In the controversy about the cause, early on there was talk of “infectious” or “rheumatic” etiology.

Alfred Bannwarth (1903 – 1970) and Heinrich Pette (1887 – 1964) argued for an allergic-hyperergic cause in the early 1940s. So they already suspected a substantial involvement of the immune system. In 1956, the Canadian Miller Fisher described another form of the disease.

He reported the course of the disease in three patients who showed acute paralysis of the eye muscles, a disturbance of the target movements (ataxia) as well as an absence of muscle reflexes in arms and legs. One patient also had paralysis of the facial musculature. Recovery occurred spontaneously in all three patients. Two years later, J. H. Austin described a chronic form of the disease, which is now called chronic inflammatory demyelinating polyneuritis (CIDP).