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LETTER TO EDITOR
Year : 2003  |  Volume : 51  |  Issue : 2  |  Page : 285

Pseudotumour cerebri and Guillain-Barre syndrome: cause or effect?


Department of Neurology, Amrita Institute of Medical Sciences and Research Center, Cochin, Kerala

Correspondence Address:
Department of Neurology, Amrita Institute of Medical Sciences and Research Center, Cochin, Kerala
ahsanmoosa@yahoo.com



How to cite this article:
Moosa A, Joy M A, Kumar A. Pseudotumour cerebri and Guillain-Barre syndrome: cause or effect? . Neurol India 2003;51:285


How to cite this URL:
Moosa A, Joy M A, Kumar A. Pseudotumour cerebri and Guillain-Barre syndrome: cause or effect? . Neurol India [serial online] 2003 [cited 2019 Dec 15];51:285. Available from: http://www.neurologyindia.com/text.asp?2003/51/2/285/1116


Sir,
We read with interest the short report by Kharbanda et al[1] on “Visual loss with papilledema in Guillain-Barre Syndrome” (GBS). The authors claim that it is a rare case of GBS with papilledema and normal CSF protein. However, certain features cast doubt about the diagnosis.
First, most reported cases of “GBS with papilledema” developed features of raised intracranial pressure (ICP) following the limb weakness unlike in this case. Second, blindness as a complication of “GBS with papilledema” has not been reported. Third, almost all the previously reported cases of “GBS with papilledema” except one had a raise in CSF protein.[2] However in this report,[2] the peripheral nerve conduction study was normal and hence does not qualify for the diagnosis of GBS. Fourth, though isolated F-waves absence is compatible with the diagnosis of early GBS, this finding is not diagnostic of the same. Fifth, exclusion of cerebral venous sinus thrombosis is mandatory in all cases of pseudotumour cerebri. In the letter to the editor for this article, Garg has proposed a few diagnostic possibilities.[3] However, we believe that the GBS like manifestation in the report by Kharbanda et al[1] is probably due to extensive radiculopathy secondary to intracranial hypertension as illustrated previously in some reports.[4],[5] Radiculopathy as a manifestation of intracranial hypertension is rare and less well known.
Obeid et al[4] reported two cases of extensive radiculopathy due intracranial hypertension; both had papilledema, marked visual impairment and flaccid areflexic quadriparesis with no parenchymal lesions on MRI of brain, brainstem and cervical spinal cord. One patient had cerebral sinus venous thrombosis and the other was diagnosed as pseudotumour cerebri. The electrophysiological findings were consistent with extensive radiculopathy. Both patients initially received intravenous immunoglobulin for GBS without benefit. But they responded well to lumboperitoneal shunting. We also reported two similar cases of angiographically proven cerebral venous sinus thrombosis presenting with rapidly progressive visual loss, ophthalmoplegia and extensive radiculopathy secondary to intracranial hypertension.[5] Despite lumboperitoneal shunting, visual outcome was poor in our cases. CSF pressure was elevated in all these cases with normal protein level.
The mechanism of radiculopathy appears to be similar to other cranial neuropathies in raised ICP. Mechanical compression of roots due to elevated CSF pressure distending the subarachnoid space around nerve roots appears to be the likely mechanism of radiculopathy. Radiculopathy secondary to raised ICP has been reported almost exclusively in patients with idiopathic intracranial hypertension or cerebral venous sinus thrombosis.[4],[5] Other causes of raised ICP may not produce diffuse increase in pressure in both intracranial and intraspinal compartments and are unlikely to manifest as radiculopathy. The constellation of flaccid-areflexic quadriplegia and papilledema may be misdiagnosed as Guillain Barre Syndrome with papilledema; such cases are under risk of inappropriate treatment.[3] Such a presentation usually signifies sustained high ICP and need urgent measures to reduce the pressure to safe levels for a better visual outcome.
In conclusion, all cases of so-called “GBS with papilledema” should be viewed with suspicion. Radiculopathy secondary to raised ICP should be considered as a differential diagnosis. Careful analysis of evolution of symptoms and electrophysiological findings, CSF protein level and pressure estimation, and appropriate vascular imaging would help to identify the correct cause.
 

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1.Kharbanda PS, Prabhakar S, Lal V, Das CP. Visual loss with papilledema in Guillain-Barre syndrome. Neurol India 2002;50:528-9.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Sullivan RL, Reeves AG. Normal cerebrospinal fluid protein, increased intracranial pressure, and the Guillain-Barre Syndrome. Ann Neurol 1977;1:108-9.  Back to cited text no. 2    
3.Garg RK. Visual loss with papilledema in Guillain-Barre syndrome. Neurol India 2003;51:135.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Obeid T, Awada A, Mousali Y, Nusair M, Muhayawi S, Memish S. Extensive radiculopathy: a manifestation of intracranial hypertension. Eur J Neurol 2000;7:549-53.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Moosa A, Kishore A, Gupta AK, Radhakrishnan K. Blindness, ophthalmoplegia and extensive radiculopathy- an unusual clinical syndrome in intracranial sino-venous thrombosis. Neurology India [In Press].  Back to cited text no. 5    

 

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