Pathogenesis of papilloedema and raised intracranial pressure in Guillain-Barre syndrome.

Reid, A.; Draper, Ivan T.

doi:10.1136/bmj.281.6252.1393

Cited by 23 publications

(20 citation statements)

References 8 publications

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“…A small number of patients develop unusual signs such as papilloedema [7] thought to be secondary to cerebral oedema and hyponatraemia [8]. Mild autonomic disturbance is seen in three quarters of patients but a few develop severe bradyarrhythmias which are recognised as a cause of infrequent death from the syndrome.…”

Section: Clinical Featuresmentioning

confidence: 99%

An Update in Guillain-Barré Syndrome

Winer

2014

Autoimmune Diseases

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Guillain-Barré syndrome (GBS) was first described in 1916 (Guillain G, 1916) and is approaching its 100th anniversary. Our knowledge of the syndrome has hugely expanded since that time. Once originally considered to be only demyelinating in pathology we now recognise both axonal and demyelinating subtypes. Numerous triggering or antecedent events including infections are recognised and GBS is considered an immunological response to these. GBS is now considered to be a clinical syndrome of an acute inflammatory neuropathy encompassing a number of subtypes with evidence of different immunological mechanisms. Some of these are clearly understood while others remain to be fully elucidated. Complement fixing antibodies against peripheral nerve gangliosides alone and in combination are increasingly recognised as an important mechanism of nerve damage. New antibodies against other nerve antigens such as neurofascin have been recently described. Research databases have been set up to look at factors associated with prognosis and the influence of intravenous immunoglobulin (IvIg) pharmacokinetics in therapy. Exciting new studies are in progress to examine a possible role for complement inhibition in the treatment of the syndrome.

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Section: Clinical Featuresmentioning

confidence: 99%

An Update in Guillain-Barré Syndrome

Winer

2014

Autoimmune Diseases

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“…Our failure to diagnose intracranial hypertension as a cause of radiculopathy in the two cases is partly due to the fact that there is a lack of its previous documentation. Though the literature contains several reports suggesting an association between PTC and GBS, such as those by Reid and Draper (1980), Behan et al (1981), Ropper and Marmarou (1984), Macay et al (1988) and Weiss et al (1991), some of these reports may be of patients similar to our own where radiculopathy was actually due to elevated intracranial pressure. The previously suggested association of GBS and PTC misled us to institute immunoglobulin therapy in both patients.…”

Section: Discussionmentioning

confidence: 72%

Extensive radiculopathy: a manifestation of intracranial hypertension

Obeid¹,

Awada²,

Mousali³

et al. 2000

Eur J Neurol

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“…2,[5][6][7] The authors of these reports explained the mechanism of increased intracranial pressure in three ways: (i) increased CSF protein concentration and osmotic pressure; (ii) obstructed CSF absorption; and (iii) brain oedema. 5,[8][9][10][11] As the ventricular CSF protein concentration is sometimes normal 12 and brain oedema causes acute hydrocephalus only when the CSF outflow is compressed, most authors support the idea that intracranial hypertension and subsequent hydrocephalus mainly results from reduced CSF absorption, which can resolve spontaneously 6,13,14 or be relieved by CSF diversion. 2,5,7 In our patient, impaired cognition was the main indication for brain imaging.…”

Section: Discussionmentioning

confidence: 98%