[Skip to Content]
[Skip to Content Landing]
Citations 0
May 19, 1999

High-Altitude Cerebral Edema

Author Affiliations

Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999

JAMA. 1999;281(19):1794. doi:10-1001/pubs.JAMA-ISSN-0098-7484-281-19-jbk0519

To the Editor: Dr Hackett and colleagues1 investigated 9 patients with HACE by MRI and found intense T2 signals in white matter areas, especially in the corpus callosum and the splenium, in 7 cases. We disagree with Hackett et al1 that these MRI findings prove that the predominant mechanism of HACE is a vasogenic edema. If the hyperintensities found in the callosal bodies of their patients had caused neurological symptoms, they would be expected to produce a hemispheric disconnection syndrome. This syndrome results in 2 isolated hemispheres that are no longer able to carry out tasks dependent on information processed in the other half of the brain. Accordingly, neither hand can match to sample an object presented visually or tactually to the ipsilateral hemisphere. Furthermore, the isolated right hemisphere fails tasks involving language such as naming objects and reading words projected to the left visual field, performing gestures with the left hand on verbal command, and naming objects held in the right hand. The clinical signs of the hemispheric disconnection syndrome consist of tactile agnosia, ideomotor dyspraxia, and agraphia of the left hand and constructional apraxia of the right hand.2 The patients described by Hackett et al showed headache, anorexia, nausea, reduced consciousness with confusion, lethargy or even coma, and ataxia. In contrast, no signs and symptoms of the hemispheric disconnection syndrome are reported, either because they were absent or because no neuropsychological examinations were done. Thus, the MRI findings reported by Hackett et al do not explain the neurological signs and symptoms found in their patients with HACE, and it is not clear whether the MRI findings were symptomatic. Consequently, the intense T2 signals in the corpus callosum and the splenium reported by Hackett et al do not prove that HACE is related to cerebral edema.

First Page Preview View Large
First page PDF preview
First page PDF preview