Introduction: High-altitude cerebral edema is a potentially fatal neurologic syndrome that develops in subjects exposed to high-altitude. It may appear associated to other forms of altitude illnesses as acute mountain sickness or high-altitude pulmonary edema. The exact pathophysiology of high-altitude cerebral edema is still unknown and there is not consensus about the primarily type of edema: vasogenic or cytotoxic. We present a patient who suffered high-altitude cerebral edema and the clinical, neuroimaging and ultrasonographic findings at first and during the follow up.
Clinical case: A 49 year old man, mountain climber, at altitude of 5,400 m presented altered mental status and ataxia with progressive neurologic deterioration, associated to pulmonary edema. After being introduced at hyperbaric chamber, patient was descended to hospital. The magnetic resonance imaging (MRI) revealed increased T2 signal in the white matter, especially in the splenium of the corpus callosum. Corticosteroids and acetazolamide were administered and patient was transferred to our hospital. Transcranial Doppler sonography (TCD-A) using acetazolamide showed an impaired cerebral vasoreactivity. Clinical improvement of the patient was fast. MRI performed 14 days after clinical onset showed partial resolution of corpus callosum lesion. MRI and TCD-A performed six months after were normal.
Conclusions: TCD-A in our patient show a diminished cerebral vasoreactivity related to high-altitude cerebral edema. These findings suggest that impairment of cerebral autoregulation might play a role in high-altitude cerebral edema pathogenesis. Reversible clinical and neuroimaging changes indicate a predominant vasogenic edema.