Acta Neurochir (2012) 154:59–62
DOI 10.1007/s00701-011-1162-7

CASE REPORT

Traumatic subarachnoid hemorrhage, basal ganglia
hematoma and ischemic stroke caused by a torn
lenticulostriate artery
Christian Fung & Werner J. Z’Graggen & Jürgen Beck &
Jan Gralla & Stephan M. Jakob & Philippe Schucht &
Andreas Raabe

Received: 8 June 2011 / Accepted: 2 September 2011 / Published online: 6 October 2011
# Springer-Verlag 2011

Abstract Subarachnoid hemorrhage (SAH), basal ganglia
hematoma (BGH) and ischemic stroke are common
diseases with diverging therapies. The simultaneous occurrence of these diseases is rare and complicates the therapy.
We report the case of a 30-year-old man with a ruptured
lenticulostriate artery after traumatic brain injury that
caused the combination of SAH, BGH and ischemic stroke
and subsequent cerebral vasospasm. This rupture mimicked
the pathophysiology and imaging appearance of aneurysmal SAH. The site of rupture was not secured by any
treatment; however, hyperdynamic therapy and percutaneous transluminal angioplasty were feasible in this setting to
prevent additional delayed neurological deficit.

Sources of funding Financial support for patient care and treatment
was provided by Bern University Hospital, Department of
Neurosurgery, Bern, Switzerland. No additional funding was received.
This work has not been previously published or presented.
C. Fung : W. J. Z’Graggen : J. Beck : P. Schucht : A. Raabe (*)
Department of Neurosurgery,
Bern University Hospital and University of Bern,
c/o Publication Office, Susan Wieting,
3010 Bern, Switzerland
e-mail: susan.wieting@insel.ch
J. Gralla
Institute of Neuroradiology, Bern University Hospital and
University of Bern,
3010 Bern, Switzerland
S. M. Jakob
Department of Intensive Care Medicine,
Bern University Hospital and University of Bern,
3010 Bern, Switzerland

Introduction
Subarachnoid hemorrhage (SAH) is a common finding in
traumatic brain injury (TBI) [5]. The incidence of basal
ganglia hematoma (BGH) based on shearing of the
lenticulostriate arteries however is not a common entity
[1, 8, 19] nor is there a wide body of literature regarding
focal ischemic lesions after TBI [4, 9, 10]. Each disease has
distinct and partially diverging therapy regimes, and the
simultaneous occurrence of all three entities complicates the
clinical course [20]. Therapy for deep-seated hematomas is
mainly conservative and includes the management of
arterial blood pressure to prevent recurrent hemorrhage,
intracranial pressure and other medical complications [2].
Treatment of ischemic stroke varies and depends on the
etiology [6]. In SAH, the two major causes are either
trauma or aneurysmal bleeding. Traumatic subarachnoid
hemorrhage (tSAH) shows distinct differences when compared to aneurysmal subarachnoid hemorrhage (aSAH) [7].
With tSAH, onset time and severity of vasospasm are
generally earlier and of milder course, respectively [13, 21].
In addition, tSAH is often located toward the convexity of
the hemisphere. However, if tSAH originates from large
vessels, radiological findings as well as the clinical course
might mimic aneurysmal hemorrhage with severe vasospasm and the need for neuro-intervention [3, 11, 12, 16,
17, 20, 21]. To our knowledge this is the first report
describing the occurrence of SAH, BGH and ischemic
stroke secondary to TBI. The aim of this report is to
describe the combination of the lesions, to highlight the
probability of severe cerebral vasospasm with severe tSAH
and the feasibility of angioplasty in the setting of a ruptured
lenticulostriate artery.

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Case report
A male patient 30 years of age was admitted after getting
into a brawl that resulted in an impact to the right side of
his head. Upon neurological examination, the patient was
disoriented to time and place, with eye opening to speech
and a left-sided hemiparesis [analogous to Glasgow coma
scale (GCS) score of 13]. A CT scan showed a SAH
analogous to aSAH Fisher grade 3 [7], an intracerebral
hematoma within the cerebral peduncle, crus posterius of
the internal capsule and the medial thalamus on the right,
and a fracture of the skull base (Fig. 1a, b).
The patient was intubated because of a drop in GCS
score and severe agitation. Assuming that a ruptured
aneurysm or an artery dissection caused the SAH, cerebral
angiography was performed on the day of admission, but
yielded no pathological results. Because of the Fisher grade
3 bleeding, treatment with nimodipine was started. The next
day the patient was extubated, still agitated and had a leftsided hemiplegia. A CT scan 20 h after admission showed,
Fig. 1 CT scan at admission
revealed typical severe SAH
predominately in the basal
cistern and Sylvian fissure (a)
following severe head trauma.
MRI revealed a hemorrhagic
lesion in the caudal aspect of the
right basal ganglia (SWI, b) and
an ischemic lesion of the right
basal ganglia in
diffusion-weighted imaging (c)
and apparent diffusion
coefficient maps (d)

Acta Neurochir (2012) 154:59–62

in addition to the initial findings, ischemic basal ganglia
infarction on the right side. Magnetic resonance imaging
(MRI) 14 h later confirmed sub-acute ischemic infarction
but showed no signs of axonal shearing injuries on T2weighted image or susceptibility weighted imaging (SWI)
despite moderate head trauma (Fig. 1b–d). In the following
days, CT scan ruled out hydrocephalus. However, transcranial Doppler (TCD) sonography showed a mild increase
of mean velocities from 780 to 1,340 mm/s (days 2 to 4) of
the left middle cerebral artery (MCA). The patient was
clinically stable, oriented to person and place with a
persisting left-sided hemiplegia [GCS 14, NIH Stroke Scale
(NIHSS) 12].
Five days after the trauma, the GCS score dropped to 12,
and the NIHSS score increased to 16. In addition, there was
an increase of mean TCD velocities of the right MCA from
930 to 3,330 mm/s (days 4 to 5). Cerebral angiography was
performed and confirmed severe vasospasm of the intracranial segments of both internal carotid arteries (ICA) and
the right MCA. Percutaneous transluminal angioplasty

Acta Neurochir (2012) 154:59–62

(PTA) for the ICA on both sides and MCA on the right side
were performed (Fig. 2). Using hyperdynamic therapy with
a mean arterial pressure of 100 mmHg, the clinical course
stabilized [15]; however, on day 8, the patient presented
with a new onset of mild hemiparesis on the right side and a
mean velocity of 2,380 mm/s of the left MCA. Cerebral
angiography was performed and again confirmed severe
vasospasm of the left MCA and the left distal ICA. Both
locations of vasospasm were treated by PTA. Right-sided
neurological deficits resolved completely after PTA, and
TCD velocity dropped significantly (1,400 mm/s). The
patient was alert and neurologically stable with a GCS
score of 14 and NIHSS score of 12 for 2 days. However, on
day 10 he had a relapse of right-sided hemiparesis (NIHSS
16) and increasing TCD velocity (2,430 mm/s) of the left
MCA. Another diagnostic angiography, followed by PTA
of both ICAs and the left MCA, was necessary in order to
restore sufficient perfusion.
The patient improved again to the initial GCS and
NIHSS scores with no clinical evidence for vasospasms
during the following days. Hyperdynamic therapy stopped
on day 14. On discharge (day 15) the patient presented with
left-sided hemiplegia but no other deficit. The highest mean
TCD velocity at discharge was 830 mm/s at the right
anterior cerebral artery (ACA).

Discussion
The combination of the various lesions consisting of SAH,
BGH and ischemia suggests a rupture of a lenticulostriate
artery. Other vascular causes for SAH and ischemia, such as
aneurysmal bleeding or traumatic artery dissection, could not
be detected with MRI and cerebral angiography. Direct
trauma-associated bleeding in the course of the skull base
Fig. 2 The digital subtraction
angiography of the right ICA
territory shows severe
vasospasm of the MCA and
ACA (a). After local
administration of 2.5 mg
nimodipine into the terminal
ICA and balloon dilatation of
the ICA and M1 segment of the
MCA distal ICA and proximal
MCA increased in diameter (b)

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fracture seemed unlikely to us since we would have expected
at least some blood in the epidural or subdural space if the
fracture had been responsible for the SAH analogous to Fisher
grade 3. To our knowledge, this is the first report of a ruptured
lenticulostriate artery that caused clinical and CT scan typical
aSAH, ischemic infarction of the basal ganglia and BGH as a
result of head trauma. Because of the typical presence of
subarachnoid and parenchymal hemorrhage, we assumed that
the rupture of the artery occurred at, or near, the branching site
from the M1 segment of the MCA and that the disruption of
blood supply caused the circumscribed ischemia in the basal
ganglia.
Treatment of this patient was intended to prevent
delayed neurological deficit as a consequence of cerebral
vasospasm. The highest risk for developing hemodynamically significant vasospasm after tSAH occurs within the
first 7–8 days after trauma [13], whereas vasospasm after
aSAH can occur up to 14 days after aneurysm rupture [18].
Additionally, mean TCD velocities are reported to be lower
after tSAH compared to aSAH [13]. In this case, however,
the highest mean TCD velocity was at day 5, and at day 10
clinical evidence and angiographically proven vasospasm
were present.
Radiological and TCD findings, as well as the need for
three treatments with PTA up to 10 days after trauma,
resemble the characteristics of cerebral vasospasm after
aSAH rather than those reported after tSAH. Although the
site of rupture was not secured, aggressive treatment of the
vasospasm was indicated in order to preserve right-sided
motor function and prevent imminent infarction. We
decided to proceed with induced hypertension as well as
endovascular angioplasty based on the results of treatment
of severe vasospasm in the presence of unsecured aneurysms [14]. Neither PTA nor hyperdynamic therapy caused
rebleeding.

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Conclusions
This case highlights (1) that a ruptured artery might mimic
the pathophysiology of aSAH with the risk of cerebral
vasospasm, (2) the necessity of neurointensive care to
monitor and treat possible delayed neurological deficits
after tSAH comparable to Fisher grade 3 and (3) that
treatment of cerebral vasospasm such as hyperdynamic
therapy and PTA seems to be feasible in the setting of a
ruptured unsecured artery.
Acknowledgments The authors received editing support for the
final manuscript by Susan Wieting, Bern University Hospital,
Department of Neurosurgery, Publication Office, Bern, Switzerland.
Conflicts of interest None.

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