Unusual presentation of more common disease/injury

CASE REPORT

Transient hemiparesis due to a ruptured cerebral
aneurysm in the prehospital setting
Youichi Yanagawa,1 Kazuoki Hirano,2 Arisa Hayashida,2 Tomoko Nakazato2
1

Department of Emergency and
Disaster Medicine, Juntendo
University Shizuoka Hospital,
Izunokuni, Shizuoka, Japan
2
Juntendo University,
Bunkyo-ku, Tokyo, Japan
Correspondence to
Professor Youichi Yanagawa,
yyanaga@juntendo.ac.jp

SUMMARY
A 67-year-old woman developed a sudden onset
headache and left hemiparesis. Emergency medical
technicians found that she was conscious, but had left
hemiparesis. On arrival, she had an isolated headache
without any neurological deficits, however, suddenly
became comatose during a head CT examination, which
demonstrated a subarachnoid haemorrhage. The head
CT angiography on the second day revealed a cerebral
aneurysm at the right middle cerebral artery, which was
clipped on the same day. The patient demonstrated left
haemiplegia and total aphasia after the operation,
however, the neurological deficit gradually subsided and
discharged on foot in 4 months without any deficits.
Some patients with a subarachnoid haemorrhage may
demonstrate transient neurological deficits, like those
occurring during an ischaemic stroke, so emergency
medical technicians and physicians should pay attention
to treat such patients gently to avoid the re-rupture of a
cerebral aneurysm, especially if the patient has headache
symptoms.

BACKGROUND
The main symptoms of a ruptured cerebral aneurysm are a sudden onset headache or unconsciousness after a headache, without any neurological
deficit. However, approximately one-third of
patients with a ruptured cerebral aneurysm demonstrate a neurological deficit based on complications
associated with an intracerebral haematoma or the
localisation of the subarachnoid haemorrhage.1
This deficit usually does not improve in the short
time during transportation from the scene to a
local hospital, and there have so far been no
reports which demonstrated any transient neurological deficit due to a ruptured cerebral aneurysm
in the prehospital setting. Hence, we report the
first case of a transient hemiparesis due to a ruptured cerebral aneurysm in the prehospital setting
and discuss the mechanism underlying this
phenomenon.

CASE PRESENTATION

To cite: Yanagawa Y,
Hirano K, Hayashida A,
et al. BMJ Case Rep
Published online: [please
include Day Month Year]
doi:10.1136/bcr-2013010321

A 67-year-old woman developed a sudden onset
headache and left hemiparesis that prevented her
from standing and walking. She had no specific
history or family history. Emergency medical technicians found that she was conscious, but had left
hemiparesis.

INVESTIGATIONS
On arrival, she remained conscious. Her vital signs
were: blood pressure 170/82 mm Hg; heart rate 84

Yanagawa Y, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-010321

bpm and percutaneous oxygen saturation on room
air 99%. The left hemiparesis subsided, but she had
an isolated headache without any neurological deficits. She suddenly became comatose during a head
CT examination, which demonstrated a subarachnoid haemorrhage (figure 1). She immediately
underwent tracheal intubation to secure her airway
after being given a sedative and muscle relaxant.
A biochemical blood examination revealed no specific changes. The head CT on the second day of
hospitalisation demonstrated a subarachnoid haemorrhage with a sylvian haematoma and CT angiography revealed two cerebral aneurysms at the right
middle cerebral and anterior communicating arteries (figure 2).

DIFFERENTIAL DIAGNOSIS
According to previous reports, the differential diagnosis for a headache with a transient neurological
deficit was a migraine with hemiparesis, dissection
of the cerebral artery, traumatic extra-axial haematoma, vasculitis or syndrome of transient headache
and neurological deficits with cerebrospinal fluid
lymphocytosis.2–8 These diseases could all be ruled
out based on the results of CT and CT angiography
in this case.

TREATMENT
After the diagnosis of a ruptured aneurysm, the
patient underwent aggressive blood pressure
control targeting under 120 mm Hg of systolic
blood pressure and was also treated for vasospasm
using nicardipine, stress control and the prevention
of convulsions using midazolam, respiratory
support with mechanical ventilation using vecuronium and the prevention of Cushing ulcer formation using ranitidine. On the second hospital day,
we clipped both aneurysms, confirming that the
middle cerebral aneurysm was the bleeding source
and evacuated the sylvian haematoma. After performing the aneurysmal clipping, cisternal drainage
of the subarachnoid haemorrhage, permissive
hypertension management and the use of fasudil
were applied; the use of nicardipine was continued
for the treatment of cerebral vasospasm, and a
dehydrator was also used to treat brain oedema.

OUTCOME AND FOLLOW-UP
The patient demonstrated left haemiplegia and
total aphasia after the operation, however, the
neurological deficit gradually subsided and the
patient was discharged on foot within 4 months
without any deficits.
1

Unusual presentation of more common disease/injury
spasm induced by a subarachnoid haemorrhage.10 The cerebral
artery can exhibit spastic changes induced by subarachnoid
haemorrhage immediately after aneurysmal rupture during the
subacute phase. Immediate transient vasospastic changes following a hemodynamic insufficient blood supply, which was rapidly
resolved by hypertension, may have caused the hemiparesis in
the prehospital setting in this case.

Learning points

Figure 1 Head CT on arrival (right) and on the second day (left). The
head CT on arrival demonstrated a diffuse subarachnoid haemorrhage.
The right sylvian fissure had a fresh subarachnoid haemorrhage during
CT examination on arrival, which was confirmed the next day.

DISCUSSION
The present case demonstrated transient left hemiparesis with a
sudden onset headache due to a ruptured middle cerebral aneurysm in the prehospital setting, and became comatose after
re-rupture of the aneurysm after she was admitted to the hospital. There has been no report which described improvement
of such deficit due to a ruptured cerebral aneurysm in the short
time during transportation from the scene to a local hospital.
The one possible mechanism causing the transient neurological
deficit was subsequent distal embolisation or parent vessel occlusion due to local extension from an intrasaccular aneurysmal
thrombosis.9 The factors associated with aneurysmal thrombosis
are the size, and particularly, the ratio of the chamber volume to
the orifice area, blood stagnation, slow flow and increased blood
viscosity.9 The aneurysmal size of the present case was less than
10 mm and the neck was narrow, so this condition was considered to be unlikely. Another possible mechanism was transient
ischaemia based on hemodynamic insufficiency due to vaso-

▸ Some patients with subarachnoid haemorrhage may
demonstrate transient neurological deficits, like those
occurring during an ischaemic stroke.
▸ Re-rupture of a cerebral aneurysm could be lethal.
▸ Emergency medical technicians and physicians should treat
such patients gently to avoid the re-rupture of a cerebral
aneurysm, especially if the patient has headache symptoms;
for example, aggressive headache control using pain killers,
stress control using sedatives and anticonvulsant medication
and blood pressure control after a diagnosis of subarachnoid
haemorrhage, are recommended to prevent any fatal
re-bleeding of the aneurysm until either aneurysmal neck
clipping or coiling can be performed.

Acknowledgements The authors would like to thank Dr Katoh who treated the
patient.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES
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9

Figure 2 A CT angiogram taken on the second day. The CT
angiogram demonstrated a cerebral aneurysm at the right middle
cerebral artery (arrow).

2

10

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Yanagawa Y, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-010321

Unusual presentation of more common disease/injury

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