Imaging Spectrum of High Altitude Cerebral Edema: MRI Findings and Proposed Severity Classification
Keywords:
High-Altitude Cerebral Edema, Hace, Magnetic Resonance Imaging, Corpus Callosum, Splenium, Diffusion Restriction, Cerebral Edema, Microbleeds, High-Altitude Illness, Leh–Ladakh.Abstract
Purpose: To evaluate the spectrum of magnetic resonance imaging (MRI) findings in patients with high-altitude cerebral edema (HACE) presenting in the Leh–Ladakh region and to assess the distribution and severity of cerebral involvement.
Materials and Method: This retrospective study included 18 patients diagnosed with HACE between 2021 and 2024 in the Leh–Ladakh region. MRI examinations were reviewed for the pattern and extent of cerebral involvement, including corpus callosal lesions, white matter abnormalities, diffusion restriction, and hemorrhagic changes on gradient recalled echo (GRE)/susceptibility-weighted imaging (SWI) sequences.
Results: The most common MRI finding was isolated involvement of the splenium of the corpus callosum, observed in 44.4% (8/18) of patients. Diffuse corpus callosal involvement was seen in 27.8% (5/18), while isolated periventricular white matter abnormalities were identified in 16.7% (3/18). Mixed involvement of the corpus callosum and cerebral white matter was present in 11.1% (2/18) of cases. Diffusion restriction, indicative of cytotoxic edema, was demonstrated in approximately 88.9% (16/18) of patients. Microbleeds on GRE/SWI sequences were detected in 22.2% (4/18) of patients and were more commonly associated with extensive disease. The corpus callosum, particularly the splenium, was the most consistently affected structure.
Conclusion: HACE demonstrates a broad spectrum of MRI manifestations ranging from isolated reversible splenial lesions to extensive white matter involvement with hemorrhagic changes. The corpus callosum, especially the splenium, is the most frequently involved structure. Recognition of these characteristic imaging patterns can facilitate early diagnosis, guide timely therapeutic intervention, and improve outcomes in individuals exposed to high-altitude environments.
References
1. Hackett PH, Roach RC. High-altitude cerebral edema. N Engl J Med. 2001;345(2):107-114.
2. Bärtsch P, Swenson ER. Acute high-altitude illnesses. N Engl J Med. 2013;368(24):2294-2302.
3. Kallenberg K, Bailey DM, Christ S, et al. Magnetic resonance imaging evidence of cytotoxic and vasogenic edema in high-altitude cerebral edema. Radiology. 2007;243(1):171-178.
4. Schommer K, Kallenberg K, Lutz K, et al. Hemosiderin deposition in the corpus callosum as a marker for high-altitude cerebral edema. J Appl Physiol. 2013;114(1):87-91.
5. Bailey DM, Bärtsch P, Knauth M, Baumgartner RW. Emerging concepts in acute mountain sickness and high-altitude cerebral edema: from the molecular to the morphological. Brain. 2009;132(Pt 2):455-465.
6. Wilson MH, Newman S, Imray CHE. The cerebral effects of ascent to high altitudes. Pract Neurol. 2009;9(4):183-190.
7. Schommer K, Kallenberg K, Lutz K, Bärtsch P, Knauth M. Hemosiderin deposition in the brain as footprint of high-altitude cerebral edema. Neurology. 2013;81(20):1776-1779.
8. Tada H, Takanashi JI, Barkovich AJ, et al. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Radiology. 2004;231(1):95-100.
