Case Report

HIGH ALTITUDE MEDICINE & BIOLOGY
Volume 00, Number 00, 2017
ª Mary Ann Liebert, Inc.
DOI: 10.1089/ham.2016.0103

Extensive Microhemorrhages of the Cerebellar
Peduncles After High-Altitude Cerebral Edema
Jacqueline Pichler Hefti,1 Philipp Hoigné-Perret,2 and Raimund Kottke3

Abstract

Pichler Hefti, Jacqueline, Philipp Hoigné-Perret, and Raimund Kottke. Extensive microhemorrhages of the
cerebellar peduncles after high-altitude cerebral edema. High Alt Med Biol 00:000–000, 2017.—Neuromagnetic
resonance imaging (MRI) of subjects who suffered from high-altitude cerebral edema (HACE) typically shows
cerebral microhemorrhages (MH) of the corpus callosum, in particular the splenium, and supratentorial white
matter. This is a case report of a 43-year-old male, who suffered from unusually prolonged severe ataxia and
amnesia after having been rescued during the ascent to Mount Everest at 6400 m. MRI of the brain 63 days after
the incident showed the typical MH in the corpus callosum, but, in addition, extensive MH were found in the
middle cerebellar peduncles. These infratentorial MH might reflect the pronounced atactic gait disorder. This
case describes the first HACE-associated MH in the cerebellar peduncles in a high-altitude mountaineer
indicating a potential vulnerability of infratentorial brain areas to hypobaric hypoxia.
Keywords: acute mountain sickness; amnesia; ataxia; cerebellar peduncle; high-altitude cerebral edema;
microhemorrhage

unremarkable and neither severe AMS nor HACE or HAPE
were reported in the past.
Our patient and three other mountaineers, who did not
know each other before, and their respective personal local
climbing guides joined to an expedition group to share expenses for climbing permit and logistics. The ascent protocol
to climb Mount Everest was in accordance with the usual
practice: after the journey from Kathmandu (1400 m) to
Everest Base Camp (5100 m) on the Tibetan side 7 days were
spent at Base Camp for acclimatization, followed by acclimatization climbs to 5600 m, 5800 m, and four more days of
acclimatization. Advanced Base Camp (6400 m) was reached
on day 11. Soon after arrival at 6400 m, the mountaineer
noted uncertainty in walking with impaired balance and
moderate left occipital headache. He did not complain about
dyspnea, severe headache, nausea, or emesis. However,
clinical deterioration proceeded with somnolence, amnesia
for an episode of 3 days, and sustained ataxia. Since there was
not strong affiliation between the expedition members, the
others proceeded with the climb. Due to the atypical presentation, which was not obviously associated with a lifethreatening condition for nonmedics, he was not immediately
evacuated. He was brought down by his local guide on a yak

Introduction

H

igh-altitude cerebral edema (HACE) is a lifethreatening complication of high-altitude stay. Symptoms include drowsiness, altered consciousness, and ataxia
(Hackett, 1999). HACE can occur in subjects with progression
of acute mountain sickness (AMS), and the risk of developing
HACE may be increased in subjects with high-altitude pulmonary edema (HAPE) due to worsening of hypoxemia in this
setting. The exact etiology of HACE and whether AMS and
HACE are caused by the same pathomechanisms is still unknown. HACE is supposed to be of vasogenic origin (Hackett
et al., 1998). Pathognomonic on imaging for blood–brain
barrier disruption in HACE is the finding of microhemorrhages
(MH) in the corpus callosum, particularly in the area of the
splenium (Kallenberg et al., 2008; Schommer et al., 2013).

Case

The 43-year-old male mountaineer planned to climb
Mount Everest from the north side in spring 2014. He is an
experienced climber and the highest peak he successfully
summited before was Mount Ama Dablam (6814 m) in 2012
with only little symptoms of AMS. His medical history is
1
2
3

Division of Pneumology, Inselspital, University and University Hospital Bern, Bern, Switzerland.
Kardiologische Gemeinschaftspraxis Bern, Bern, Switzerland.
Radiology, Kinderspital Zurich, University Children’s Hospital, Zurich, Switzerland.

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PICHLER HEFTI ET AL.

to Base Camp after these 3 days, where he was examined by a
doctor, but communication was impossible due to language
problems. He received no specific medical therapy, especially no dexamethasone which would have been indicated in
HACE. Although oxygen was administered, somnolence and
ataxia persisted over another 10 days before the symptoms
resolved. He left Base Camp after these 10 days after weather
conditions had improved and he had received the authority
permit to travel to Nepal. He returned to Switzerland on his
own, without medical assistance.
Back home, the mountaineer sought medical advice.
Clinical inspection nearly 2 months after the incident revealed a well-trained general condition. Neurological examination showed no signs of cerebellar abnormalities with a
normal finger-to-nose test, diadochokinesia, motility of the
eyes, and regular gait. Neurocognitive and neurophysiological examinations were not performed.
Although the retrospective diagnosis of HACE was very
likely, contrast-enhanced magnetic resonance imaging (MRI)
of the brain at 3 Tesla was additionally performed to rule out
other cerebral alterations. On the susceptibility weighted
imaging sequence multiple small hypointensities, most likely
representing MH were found in the corpus callosum, deep
white matter of the centrum semiovale, and the middle cerebellar peduncles (MCP) in a symmetrical distribution
(Figs. 1–3). The most pronounced affection was seen in
the genu and splenium of the corpus callosum and in the
MCP. The superior and inferior cerebellar peduncles were

FIG. 2. Multiple MH in the splenium (white arrow) and
the genu of the corpus callosum (small arrows) typical for
HACE. HACE, high-altitude cerebral edema.

FIG. 1. Symmetric distribution of MH in the deep white
matter (short arrows) and the corpus of the corpus callosum
(long arrows). MH, microhemorrhages.

FIG. 3. Multiple MH in both middle cerebellar peduncles
(white arrows). Black arrowhead indicates old cystic hemorrhagic defect.

CEREBELLAR PEDUNCULAR MICROHEMORRHAGES IN HACE

not affected. On T1-weighted, T2-weighted, and fluidattenuated inversion recovery images, signal of the brain
parenchyma was normal with the exception of a cystic parenchymal defect of the vermis and adjacent left cerebellar
hemisphere. The lesion showed gliotic changes and peripheral susceptibility artifacts in keeping with small hemosiderin
deposits (Fig. 3). There were no signs of subacute bleeding.
In a follow-up MRI after 1 year, the lesion, vermis, and
cerebellar hemisphere presented completely unchanged and
thus was considered an incidental finding, most likely corresponding to a residuum of an old, possibly even prenatal,
hemorrhage or infarct and was not related to MH and HACE.
The MH were unchanged in number and distribution on
follow-up imaging, at best a slight haziness of some MH was
observed. Both examinations were performed on a 3 Tesla MR
unit (MAGNETOM Skyra; Siemens, Erlangen, Germany).
Discussion

The course of the events and symptoms are strongly suggestive for HACE, although information on the case history is
limited due to the 3-day amnesia and statements of a third
party are missing. In this case, it is rather unusual, that no
mild-to-severe AMS was reported earlier and that gait ataxia
was very pronounced and persisted for an uncommonly long
time. And, although the severity of symptoms was alarming,
it is exceptional that no fatal progression occurred with the
delayed treatment that was restricted to oxygen supply, only.
In line with typical findings on neuroimaging in subjects
who suffered from HACE, we found MH in the corpus callosum and cerebral white matter of the centrum semiovale
(Figs. 1 and 2). But, in addition, multiple infratentorial MH
were present in the MCP (Fig. 3) indicating major blood–
brain barrier dysfunction in this area, a finding, which has not
been described before in the context of HACE. The amount of
MH in our case is comparable to the images published by
Schommer and Kallenberg in patients who suffered from
severe HACE (Schommer et al., 2013).
It has been shown that vasogenic edema is the major factor
in the pathophysiology of HACE (Hackett, 1999). Vasogenic
edema, indicating blood–brain barrier disruption, occurs with
a predilection for the splenium of the corpus callosum and
deep white matter and can lead to MH. In the study of Hackett
(1999), no mention of symmetric vasogenic edema in the
cerebellar peduncles has been made. The reason for these
predilection sites is unknown, but it is assumed that vasogenic edema is more likely to occur in white matter due to its
orderly structure. A possible common feature of the corpus
callosum and the MCP may be that in both sites white matter
fibers are highly structured. Vasogenic edema of the MCP is
not very common but has been described in other pathologies
affecting the blood–brain barrier as in posterior reversible
encephalopathy (Morales and Tomsick, 2015).
The corpus callosum is supplied by short perforating arteries, whereas the MCP are mainly supplied by the anterior
inferior cerebellar arteries, so the vascular supply of both
structures does not readily explain the common findings in
our case.
The patient’s history did not reveal any previous episodes of
severe AMS or HACE, although little AMS symptoms have
been reported in the context of an earlier mountain expedition.
Therefore, and as there is some evidence for cerebral MH in
asymptomatic but severely hypoxemic mountaineers at high

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altitude (Kottke et al., 2015), it cannot be excluded that some
of the MH may have been preexisting from a previous sojourn
to high altitude. Ataxia is a common symptom in HACE, in
this case severity and duration of gait ataxia were very pronounced. This somehow unusual presentation might be reflected by the exceptional peduncular MRI findings.
Conclusion

This case demonstrates that MH in the setting of HACE
may also occur in an infratentorial location in the MCP, in
addition to the classic affection of the corpus callosum and
supratentorial white matter of the centrum semiovale. Furthermore, these findings suggest the MCP to be an additional
predilection site of hypoxemic or HACE-induced blood–
brain barrier disruption. Both, the corpus callosum and the
MCP are highly ordered white matter structures, which may
make them more susceptible to vasogenic edema and ultimately MH under certain conditions. We can only hypothesize that the prolonged stay at high altitude after symptom
onset and the lack of adequate treatment are etiologic for the
unusual pattern of MH in our case. The exact pathophysiology remains to be elucidated. Future MRI studies will show
whether involvement of the MCP in HACE as in this case is
rare or actually more common than currently thought.
Author Disclosure Statement

No competing financial interests exist.
References

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Address correspondence to:
Jacqueline Pichler Hefti, MD
Division of Pneumology
Inselspital
University and University Hospital Bern
Bern 3010
Switzerland
E-mail: jacqueline.pichler@insel.ch
Received August 31, 2016;
accepted in final form December 16, 2016.