Acute and Evolving MRI of High-Altitude Cerebral Edema: Microbleeds, Edema, and Pathophysiology

Abstract

MR imaging of high-altitude cerebral edema shows reversible WM edema, especially in the corpus callosum and subcortical WM. Recent studies have revealed hemosiderin deposition in WM long after high-altitude cerebral edema has resolved, providing a high-altitude cerebral edema "footprint." We wished to determine whether these microbleeds are present acutely and also describe the evolution of all MR imaging findings. In 8 patients with severe high-altitude cerebral edema, we obtained 26 studies: 18 with 3T and 8 with 1.5T scanners, during the acute stage, recovery, and follow-up in 7 patients and acutely in 1 patient. Imaging confirmed reversible cytotoxic and vasogenic WM edema that unexpectedly worsened the first week during clinical improvement before resolving. The 3T SWI, but not 1.5T imaging, showed extensive microbleeds extending beyond areas of edema seen acutely, which persisted and with time coalesced. These findings support cytotoxic and vasogenic edema leading to capillary failure/leakage in the pathophysiology of high-altitude cerebral edema and provide imaging correlation to the clinical course.

Fig 1.

Supine portable chest radiograph of patient 3 on admission to the hospital showing marked pulmonary edema.

Fig 2.

Patient 7, day 5, 1.5T. Axial FLAIR, diffusion, and ADC map images demonstrate hyperintensity and restricted diffusion in the entire corpus callosum and patchy areas of bilateral subcortical WM.

Fig 3.

Patient 7, 1.5T on days 5 and 10, 3T at 10 years. Axial FLAIR, diffusion, and ADC images. FLAIR hyperintensity in the corpus callosum slightly increases at day 10 and then resolves at 10 years. Restricted diffusion in the corpus callosum decreases at day 10 and resolves at 10 years. Low signal in the genu and splenium of corpus callosum on the FLAIR images at 10 years is due to hemosiderin.

Fig 4.

Patient 2. SWI. Diffuse microbleeds with a predilection for WM tracts, including the corpus callosum and middle cerebellar peduncles and subcortical WM.

Fig 5.

Patient 5, 3T. Hemosiderin-sensitive sequences at 3 days, 8 months, and 2 years. Note uniformly distributed petechial hemorrhages that persist and become more confluent with time.

Fig 6.

Patient 7. Hemosiderin-sensitive gradient echo with 1.5T on day 5 and SWI on 3T at 10 years. Microbleeds are not apparent on 1.5T. Confluent hemosiderin staining is seen in the corpus callosum at 10-year follow-up.