[Mati]

Hi Azure,
Thanx azure for interest.
I would like to give the article presented and letters in response to this article and author’s reply.

Dr Soni Srivastav is an IOM graduate and is involved in MMSN.
Dr Devish is also IOM graduate and Founder Treasurer of MMSN while he was in Third Year of his MBBS.

Prof Buddha Basnyat is one of the leaders in Mountain Medicine in the world. He is the founder president of MMSN. The web page of the society is:

www.mmsn.org.np

SORRY azure I could not upload the file from xenomed despite very try. I hope angel will do that job. I hope posted the letters. If you need more, let me know.


THE LETTERS OF THE ARTICLE:

Vol. 281 No. 19, May 19, 1999
Letters
High-Altitude Cerebral Edema
To the Editor: Dr Hackett and colleagues1 elegantly elucidate the clinical imaging correlate with the pathophysiology of high-altitude cerebral edema (HACE). However, given the setting, the diagnosis of HACE is usually clearly clinical. This point was not emphasized in the article, which inadvertently may encourage physicians to obtain magnetic resonance images (MRIs) in countries like Nepal where people with HACE in the mountains are evacuated to Kathmandu.
The cost issue is relevant especially because many high-altitude locations are in developing countries where there is no health insurance for local people and many trekkers have no insurance either. An MRI is expensive for an individual to pay for out-of-pocket.
Buddha Basnyat, MD, MSc
Himalayan Rescue Association and Nepal International Clinic
Kathmandu
1. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280:1920-1925. ABSTRACT/FULL TEXT

To the Editor: The MRI studies of patients with HACE reported by Dr Hackett and colleagues1 suggest that the major mechanism for development of the syndrome is vasogenic, ie, requiring movement of fluid and protein out of the vascular compartment. Older reports support their conclusion. In studies of serum proteins and thyroid hormones in subjects taken abruptly from sea level to 4300 m, I reported a rapid and marked increase in serum albumin and thyroxine-binding protein concentrations at high altitude and suggested plasma dehydration as the cause.2 In another study,3 my colleagues and I reported a 13.2% and 19.6% decrease in plasma volume after 4 and 8 days at 4300 m, respectively, in subjects previously acclimatized at 1610 m. Since total body water was unchanged at 4300 m, we suggested that body water redistributes at high altitude out of the plasma in favor of interstitial or intracellular spaces.
Martin I. Surks, MD
Albert Einstein College of Medicine
Bronx, NY
1. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280:1920-1925. ABSTRACT/FULL TEXT
2. Surks MI. Elevated PBI, free thyroxine, and plasma protein concentration in man at high altitude. J Appl Physiol. 1966;21:1185-1190. FULL TEXT
3. Surks MI, Chinn KSK, Matoush LR. Alterations in body composition in man after acute exposure to high altitude. J Appl Physiol. 1966;21:1741-1746. FULL TEXT

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.
Ralf W. Baumgartner, MD
University Hospital
Zurich, Switzerland
1. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280:1920-1925. ABSTRACT/FULL TEXT
2. Geschwind N, Kaplan E. A human cerebral disconnection syndrome. Neurology. 1962;12:675-685. ISI

In Reply: We entirely agree with Dr Basnyat that HACE is a clinical diagnosis generally not requiring MRI, which is expensive and often unavailable. Magnetic resonance imaging may be helpful, however, when the diagnosis is unclear. The purpose of our study was to use MRI to understand the pathophysiology, not to advocate MRI as essential for diagnosis.
The findings published by Dr Surks 33 years ago have been confirmed in many subsequent studies. The mechanism of this shift of fluid from the vascular space on ascent to high altitude and the exact division of the fluid between the intracellular and interstitial spaces are not as clear. Nor is it known whether the brain participates in this fluid translocation to the same extent as other tissues. The studies done by Surks et al were in persons without altitude illness. In those who are ill with acute mountain sickness, a net fluid retention or antidiuresis also takes place, which would aggravate any fluid shift into the brain that might be taking place and contribute to cerebral edema. However, the fluid shift from the vascular space does not, in itself, provide a clue as to whether and to what extent the brain is involved, and as to whether the brain edema is cytotoxic (intracellular) or vasogenic (blood-brain barrier leak of proteins and water).
We disagree with Dr Baumgartner that the absence of a hemispheric disconnection syndrome is evidence against a vasogenic edema. The 2 are unrelated. We are well aware of the disconnection syndrome and since discovering the finding of splenial edema, we have been looking for it. However, our patients are in no condition for such testing while acutely ill; many are unconscious. Recently, our colleague Dr Ron Kramer of Denver, Colo, examined a patient with HACE (and high-altitude pulmonary edema) 10 days after the acute illness, when the brain MRI showed splenial edema, and found no evidence of a disconnection syndrome. Sophisticated testing earlier in the course of the illness is necessary before concluding the disconnection syndrome is not present to some degree. It should not be surprising, however, that involvement of a small portion of the corpus callosum with reversible edema (as opposed to stroke, for example) may not be reflected in a disconnection syndrome. We think that the symptoms of HACE are due to intracranial pressure increase, for which there is much clinical and autopsy evidence. The cause of death is brain herniation. We did not mean to imply that HACE is due to corpus callosum dysfunction. The reversible high T2 signal in the white matter is indicative of vasogenic edema in HACE.
Peter Hackett, MD
St Mary's Hospital
Grand Junction, Colo
Phil Yarnell, MD
University of Colorado School of Medicine
Denver
Edited by Margaret A. Winker, MD, Deputy Editor, and Phil B. Fontanarosa, MD, Interim Coeditor.
JAMA. 1999;281:1794.