Margaret A.WinkerMD, Deputy EditorIndividualAuthorPhil B.FontanarosaMD, Interim CoeditorIndividualAuthor
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.
Baumgartner RW. High-Altitude Cerebral Edema. JAMA. 1999;281(19):1794. doi:10-1001/pubs.JAMA-ISSN-0098-7484-281-19-jbk0519