Unusual presentation of more common disease/injury

CASE REPORT

High-altitude cerebral oedema mimicking stroke
Uday Yanamandra,1 Amul Gupta,2 Sagarika Patyal,3 Prem Prakash Varma4
1

Department of Internal
Medicine, 153 General
Hospital, Leh, Jammu &
Kashmir, India
2
Department of Radiology,
153 General Hospital, Leh,
Jammu & Kashmir, India
3
Department of
Ophthalmology, 153 General
Hospital, Leh, Jammu &
Kashmir, India
4
Department of Medicine,
Northern Command Medical,
Leh, Jammu & Kashmir, India
Correspondence to
Dr U Yanamandra,
udayj2@gmail.com,
udayj2@yahoo.com
Accepted 21 February 2014

SUMMARY
High-altitude cerebral oedema (HACO) is the most fatal
high-altitude illness seen by rural physicians practising in
high-altitude areas. HACO presents clinically with
cerebellar ataxia, features of raised intracranial pressure
(ICP) and coma. Early identification is important as delay
in diagnosis can be fatal. We present two cases of
HACO presenting with focal deficits mimicking stroke.
The first patient presented with left-sided hemiplegia
associated with the rapid deterioration in the sensorium.
Neuroimaging revealed features suggestive of vasogenic
oedema. The second patient presented with monoplegia
of the lower limb. Neuroimaging revealed perfusion
deficit in anterior cerebral artery territory. Both patients
were managed with dexamethasone and they improved
dramatically. Clinical picture and neuroimaging closely
resembled acute ischaemic stroke in both cases.
Thrombolysis in these patients would have been
disastrous. Recent travel to high altitude, young age,
absence of atherosclerotic risk factors and features of
raised ICP concomitantly directed the diagnosis to
HACO.

ambient air. Neurologically he was found to be disoriented, non-coherent and had left-sided hemiplegia (video 1A). Respiratory evaluation revealed a
respiratory rate of 32/min and chest examination
revealed bilateral basal crepitations (right>left).
Other systemic examination was normal. Fundus
examination revealed papilledema.

Investigations
His haematological parameters and biochemical
parameters were within normal limits (haemoglobin

BACKGROUND
High altitude is associated with a variety of physiological changes in the body primarily due to
hypoxia and associated changes in barometric pressure and temperature. Lack of acclimatisation can
lead to a variety of medical problems, especially
acute mountain sickness (AMS), high-altitude cerebral oedema (HACO) and high-altitude pulmonary
oedema (HAPO).
HACO is the most fatal high-altitude illness seen
by rural physicians practising in high-altitude areas.
HACO, primarily a clinical entity, occurs in a
patient of AMS or HAPO and is characterised by
sudden-onset ataxia, altered consciousness or both.
Early identification is important as delay in diagnosis can be fatal. Focal neurological deficit is not a
usual feature of HACO. We report two cases of
HACO who presented with deficits mimicking
stroke which resolved by the resolution of cerebral
oedema.

CASE PRESENTATION
Case 1

To cite: Yanamandra U,
Gupta A, Patyal S, et al.
BMJ Case Rep Published
online: [ please include Day
Month Year] doi:10.1136/
bcr-2013-201897

A 23-year-old man was inducted to high altitude
(11 800 ft) on 12 September 2012. On the third
day of his acclimatisation (14 September 2012), he
was observed to have an unsteady gait by his colleagues. Within the next few hours, he was found to
be drowsy and not responding to verbal commands
and hence brought to our hospital. Examination on
arrival to our hospital: pulse was 84/min, blood
pressure 132/82 mm Hg, and SpO2 was 62% in

Yanamandra U, et al. BMJ Case Rep 2014. doi:10.1136/bcr-2013-201897

Video 1 (A) The patient described in case 1 on arrival
to our hospital. Observe that the individual is unable to
move the left half of his body even on painful stimulus.
(B) The patient described in case 1 at the time of
discharge.
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Unusual presentation of more common disease/injury

Figure 1 Chest radiograph on the day of admission (case 1) depicting
fluffy air space opacities in the right mid and lower zone consistent
with high-altitude pulmonary oedema.
13.2 g/dL, total leucocyte count 10 500/μL, differential leucocytes polymorphs 68%, lymphocytes 24%, blood sugar fasting/
postprandial 84/112 mg/dL, urea/creatinine 28/1.0 mg/dL, total
cholesterol 182 mg/dL). Chest radiograph revealed fluffy airspace opacities in right mid and lower zones consistent with
high-altitude pulmonary oedema (HAPO; figure 1). Optic nerve
sheath diameter (ONSD) was 11 mm. Non-contrast CT scan
(NCCT) of the brain showed diffuse cerebral oedema involving
white matter of bilateral cerebral hemispheres, mass effect in the
form of the effacement of the overlying sulci and compression
of the lateral ventricles and third ventricle. The corpus callosum
was also hypodense due to oedema. Accentuation of grey–white
matter differentiation was suggestive of vasogenic oedema
(figure 2).

Differential diagnosis

Figure 3 Chest radiograph on day 3 of admission (case 1) showing
resolution of air space opacities seen on D1 roentgenogram.

Treatment
The patient was managed with oxygen by venturi-mask at
6 L/min and parenteral dexamethasone 8 mg q8 h.

Outcome and follow-up
His cognitive functions started improving within 4 h and hemiplegia within 12 h. However, ataxia improved slowly, and by the
third day of hospitalisation, his chest was clear and his gait was
normal (video 1B). Repeat chest radiograph on the third day of
admission showed complete resolution of the opacities
(figure 3). Repeat NCCT performed on the fourth day showed
that the white matter oedema had subsided with decreased mass
effect and the grey–white matter differentiation was seen to be
normal (figure 4). He was discharged on the tenth day, and at
that time, his ONSD was 4.5 mm and papilledema had
subsided.

A clinical possibility of stroke/central venous thrombosis (CVT)
was considered due to focal neurological deficit.

Figure 2 Non-contrast CT of the head on the day of admission
(case 1) reveals diffuse cerebral oedema with mass effect effacing the
sulci and compressing bilateral lateral ventricles. Grey–white matter
differentiation is also accentuated.
2

Figure 4 Repeat non-contrast CT on day 4 of admission (case 1)
showing resolution of cerebral oedema and mass effect. Grey–white
matter differentiation has normalised.
Yanamandra U, et al. BMJ Case Rep 2014. doi:10.1136/bcr-2013-201897

Unusual presentation of more common disease/injury

Figure 6 Chest radiograph on the day of admission (case 2) depicting
fluffy air space opacities in the right mid and lower zone consistent
with high-altitude pulmonary oedema.

Figure 5 The patient described in case 2 depicting difficulty in lifting
the right lower limb due to monoplegia.

CASE PRESENTATION
Case 2
A 21-year-old man was inducted into high altitude (18 000 ft) on
7 May 2013. On the fifth day of his arrival to this altitude (12
May 2013), he presented with sudden onset of weakness of the
right lower limb on waking up from sleep (figure 5).
Examination revealed SpO2 of 52% (on ambient air); neurologically, he had monoplegia of right lower limb while the rest of the
neurological examination was found to be normal. Chest examination revealed a respiratory rate of 36/min and bilateral crepitations up to the middle of the chest. Other systems were normal.

admission showed complete resolution of the opacities (figure 8).
Repeat CT perfusion performed on the seventh day showed that
the perfusion defects had reversed, white matter oedema had
subsided with decreased mass effect, and the grey–white matter
differentiation was normal (figure 9). Power in the right lower
limb became normal (5/5 power, both lower limbs; figure 10).
He was discharged on the fourteenth day, his ONSD was 4.2 mm
at the time of discharge.

DISCUSSION
The incidence of HACO in HAPO varies from 14 to 50%. It
can occasionally present in the absence of AMS, when it is

Investigations
His haematological parameters and biochemical parameters were
within normal limits. Chest radiograph revealed fluffy air space
opacities in bilateral mid and lower zones, consistent with HAPO
(figure 6). ONSD was 12 mm. NCCT scan did not reveal any evidence of acute/ sub-acute/old infarction or haemorrhage, but had
features of vasogenic oedema with mass effect, as seen in case 1.
CT perfusion scan of the brain showed perfusion deficit in the
anterior cerebral artery (ACA) territory bilaterally (figure 7).

Differential diagnosis
A clinical possibility of stroke or CVT was considered.

Treatment
The patient was managed with oxygen by venturi mask at
6 L/min and parenteral dexamethasone 8 mg q8 h.

Outcome and follow-up
Within 12 h of initiation of the treatment, monoplegia started
improving. Repeat chest radiograph on the third day of
Yanamandra U, et al. BMJ Case Rep 2014. doi:10.1136/bcr-2013-201897

Figure 7 CT perfusion imaging on day 1 of the hospitalisation
(case 2) revealing reversible perfusion defects in the anterior cerebral
artery territory.
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Unusual presentation of more common disease/injury

Figure 8 Chest radiograph on day 3 of admission (case 2) showing
resolution of air space opacities seen on D1 roentgenogram.
particularly dangerous.1 In our patients, HACO was coexisting
with HAPO, but there were no features of AMS. HACO is a
sequence of cerebral effects of high altitude, which can progress
to a life-threatening encephalopathic stage. A prevalence of 0.5–
1.0% of HACO is observed in individuals reaching a height
>4500 m.2
Pathophysiologically, increased hydrostatic pressure, cytokines
or chemical mediators damage vessel walls, leading to microhaemorrhages in HACO. These microhaemorrhages are usually
seen only in individuals of non-fatal HACO, but not with AMS.
These haemorrhages can be seen many months after the acute
attack and are generally present in corpus callosum.3 Owing to
increased permeability of the blood–brain barrier, intracellular
and extracellular water accumulation takes place, leading to
cerebral oedema.4 5 Evidence of cerebral oedema has been seen
in the autopsies of military personnel and trekkers who had
died of HACO.6 Ring haemorrhages have also been seen in autopsies of individuals who expired due to HACO.7
The oedema in HACO is generally due to blood–brain barrier
leakage and is vasogenic in aetiology. The CT findings in HACO

Figure 9 CT perfusion imaging on day 5 of the hospitalisation
(case 2) revealing reversible perfusion defects in the anterior cerebral
artery territory.
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Figure 10 The patient described in case 2 showing normal power in
both lower limbs after the treatment.

are: diffuse hypodense appearance of the entire cerebrum with
small compressed ventricles and cisterns, and disappearance of
sulci. The CT findings in our patient correlate with the vasogenic type of oedema. MRI is much more sensitive than CT in
detecting early changes of HACO in brain parenchyma. The
characteristic findings on MRI are vasogenic oedema and
increased T2 signal in the white matter, especially in the splenium of the corpus callosum and no grey matter oedema.
The non-invasive technique of optic nerve sheath ultrasonography allows measurement of ONSD, which correlates with
intracranial pressure (ICP). Measurement of ONSD has a stronger association in the presence of AMS and correlates with the
severity of AMS than any prior assessment tool. The physiological basis of this technique is that increase in ICP is transmitted by the cerebrospinal fluid down the perineural subarachnoid
space of the optic nerve, causing an expansion of the nerve
sheath that can be measured by ultrasound.8 In our cases,
patients had increased ONSD (normal <5 mm) which subsided
to normal with treatment.
HACO generally presents with headache, change in level of
consciousness (70%), unsteady gait (61%), breathlessness, lethargy and other behavioural changes, which can later progress to
coma and death.9 Other neurological features noted in a case
series of 44 patients by Dickson et al include, papilledema
(52%), urinary retention or incontinence (48%), abnormal
Yanamandra U, et al. BMJ Case Rep 2014. doi:10.1136/bcr-2013-201897

Unusual presentation of more common disease/injury
plantar reflexes (34%), abnormal limb tone and power (14%),
abducens nerve palsy, pupil difference, visual field loss, speech
difficulty, hearing loss and flapping tremor.10 Other neurological
findings, as observed during high-altitude ascent in many
studies, include impairment of memory,11 metamemory,12 psychomotor skills,13 14 cognition, learning, language, perception
and mathematics.15 These neuropsychological changes generally
relate to rate and height of ascent. Focal neurological deficit
simulating stroke, as seen in our cases, has rarely been reported.
The pathophysiology explaining the presentation of our patients
(hemi/ monoplegia) remains conjectural. In the absence of MRI,
it would be difficult to comment on the exact aetiopathogenesis.
Possibly, raised ICP could have led to transient ischaemic attack,
which promptly reversed with appropriate therapy. False localisation, secondary to uncal herniation, can explain long-tract
signs in patients with cerebral oedema. In our case, CT scan
during the neurological deficit did not reveal any herniation.
The perfusion deficits in the second case, with the presentation of lower limb weakness, may be due to ACA territory
ischaemic infarction. However, recent arrival to high altitude,
associated features of HAPO, absence of vascular comorbidities,
age of the individual and presence of associated evidence of
vasogenic oedema point to a diagnosis of HACO. The decisionmaking in such cases becomes difficult when treatment for the
two conditions is divergent. Thrombolysis in HACO would
have led to haemorrhagic transformation and at the other end
dexamethasone is not advisable in case of ischaemic stroke. The
second case raises the possibility of vascular compression and
perfusion defects as a probable aetiology for neurological

manifestations in HACO, which needs to be evaluated in larger
studies.
The recovery time in HACO has been reported to be 3–
14 days15 and average time of 2.4 weeks in series by Hackett
et al.5 In our case, patients were hospitalised for 14 days with
complete functional and radiological recovery achieved by days
3–5 of admission.
Acknowledgements Director General Armed Forces for the support in
management of high-altitude illnesses.
Contributors UY, AG, SP and PPV were all involved actively in managing the
patients. UY prepared the manuscript and is responsible for submitting the paper.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES
1
2
3
4
5

6

7
8

Learning points

9
10

▸ Careful differentiation between stroke and high-altitude
cerebral oedema (HACO) is important in rural high-altitude
medical practice.
▸ HACO can present with reversible focal neurological deficits
mimicking stroke.
▸ Thrombolysis is contraindicated if HACO exists.
▸ Prompt therapy can lead to complete recovery of deficits in
these patients

11
12
13
14
15

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Virues-Ortega J, Buela-Casal G, Garrido E, et al. Neuropsychological functioning
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