Neurosurg Focus 26 (6):E5, 2009

Decompressive surgery in malignant dural sinus thrombosis:
report of 3 cases and review of the literature
Luigi A. Lanterna, M.D., Ph.D.,1 Paolo Gritti, M.D., 2 Ornella Manara, M.D., 3
Gianluca Grimod, M.D.,1 Gianmario Bortolotti, M.D., 2and Francesco Biroli, M.D.,1
Departments of 1Neuroscience and Surgery of the Nervous System, 2Neuroanesthesiology, and
3
Neuroradiology, Ospedali Riuniti, Bergamo, Italy
Cerebral venous and dural sinus thrombosis (CVDST) is a rare cause of stroke in young and middle-aged adults.
When the clinical course is complicated by uncontrollable intracranial hypertension and brainstem compression
due to edema or cerebral hemorrhage, the prognosis is poor. The authors evaluated the therapeutic role of surgical
decompression in patients with clinical signs of impending herniation. Cerebral venous and dural sinus thrombosis
complicated by impending brain herniation a very rare, life-threatening but potentially treatable clinical condition.
Three patients with pupillary signs of transtentorial herniation due to brain edema and hemorrhage caused by
CVDST (superior sagittal sinus in 1 patient and transverse and sigmoid sinus in 2 patients) were treated surgically.
The intervention consisted of clot removal, infarcted tissue resection, and frontotemporoparietooccipital craniectomy
with duraplasty. According to the Glasgow Outcome Scale, 2 patients were classified as having good recovery and
1, moderate disability. The results of neuropsychological assessment were normal in 2 patients and demonstrated a
partial neuropsychological deficit (neglect) in the other.
Surgery may be indicated in selected patients with CVDST whose condition is deteriorating because of intractable intracranial hypertension and impending brain herniation. (DOI: 10.3171/2009.3.FOCUS0910)

C

Key Words
•
cerebral venous thrombosis
•
craniectomy
intracranial pressure
•
dural sinus
•
hemorrhagic infarct

erebral vein and dural sinus thrombosis predominates in young and middle-aged adults. Despite
improvements in diagnosis and treatment, more
than 15% of patients remain permanently disabled or
die.7,9 Recently, the International Study on Cerebral Vein
and Dural Sinus Thrombosis (ISCVT) has shown that the
most common mechanism of acute death is transtentorial herniation due to hemorrhagic lesions or diffuse brain
edema.1,2 In these circumstances, decompressive surgery
(DS) may be the treatment to choose as it promptly creates space for swelling cerebral tissue and may also improve perfusion of collateral leptomeningeal vessels.
The ISCVT suggested the importance of investigating DS with randomized trials.7 However, the rarity of the
pathology (5 cases per million),1 and the fact that only a
minority of patients with CVDST suffer from impending brain herniation necessitating DS, means that such a
study is unlikely to succeed, even with long-term international collaborative efforts.
We report the cases of 3 patients with pupillary signs
of impending brain herniation secondary to CVDST who
underwent DS on an emergency basis, and we discuss the

Abbreviations used in this paper: CVDST = cerebral venous
and dural sinus thrombosis; GOS = Glasgow Outcome Scale; ICP =
intracranial pressure; ISCVT = International Study on Cerebral Vein
and Dural Sinus Thrombosis.

Neurosurg. Focus / Volume 26 / June 2009

•

stroke

•

rationale and the clinical results of the procedure in relation to the physiopathology of CVDST.
Source of Data

Methods

We reviewed a prospectively collected database of
the patients admitted for cerebrovascular pathological
conditions to the Neurosurgical Intensive Care Unit of
the Ospedali Riuniti of Bergamo from January 2006 to
November 2008. A patient was eligible if a diagnosis of
CVDST was confirmed by angiography, CT venography,
MR imaging, or autopsy. Exclusion criteria were: age < 18
years, cerebral lesions other than those related to CVDST,
and posttraumatic, postinfective, or iatrogenic CVDSTs.

Causal Treatment (Anticoagulation Therapy)

Causal treatment was started at the diagnosis of
CVDST and consisted of low-molecular-weight heparin
(Nadroparin) in a dose of approximately 180 anti–factor
Xa units/kg per 24 hours or dose-adjusted intravenous
heparin with an at least doubled activated partial thromboplastin time. Cerebral hemorrhage was not a contraindication against causal treatment. Patients in critical condition who could become potential surgical candidates
were preferentially treated with unfractionated heparin
because it has the advantage of being promptly antago1

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L. A. Lanterna et al.

Fig. 1. Case 1. A and B: Preoperative CT revealing a hemorrhagic infarction of the right temporal lobe with midline shift and
transtentorial herniation brainstem compression.
C and D: Preoperative CT angiograms demonstrating the non-opacification
of the transverse sinus on the right side. The arrowheads indicate the transverse sinus sulcus.    E: Preoperative CT angiogram
in frontal projection showing the non-opacification of the jugular bulb on the right side; the jugular foramens are symmetrical. The
arrowheads indicate the jugular foramen.    F and G: Postoperative CT obtained after the second operation.

nized. In the other patients, low–molecular-weight heparins were preferred because they appear to be as effective
as unfractionated heparin, they cause fewer hemorrhagic
complications, and they can be given at fixed doses without constant laboratory monitoring.4,14 The anticoagulation
therapy was never interrupted. It was maintained with a
half dosage for the first 24–72 hours after surgery (during
the period of major postoperative hemorrhage risk).8 The
2

temporary reduction of dosage is in accordance with the
guidelines of both the European Federation of Neurological Societies and the ISCVT treatment protocol, which
suggest the temporary interruption of anticoagulation
therapy in the event of invasive procedures.4,6
Decompressive Surgery

Indications for DS included: progressive neurologiNeurosurg. Focus / Volume 26 / June 2009

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Craniectomy and dural sinus thrombosis
cal deterioration unresponsive to causal treatment and
conventional intensive care (osmotherapy, moderate hyperventilation with a pCO2 of 30–35 mm Hg and hypothermia with a target temperature of 33–35°C) and CT
signs of space-occupying lesions with midline shift or
obliteration of the basal cisterns and pupillary signs of
transtentorial herniation. Written consent for surgery was
obtained from the patient or his or her next of kin. Decompressive surgery was defined in terms of external and
internal decompression. External decompression was defined as a hemicraniectomy with duraplasty (diameter ≥
12 cm), and internal decompression consisted of resecting
the infarcted brain tissue and draining cerebral hematomas. External decompression was primarily indicated in
the event of diffuse hematomas infiltrating edematous,
potentially still viable, eloquent brain, whereas internal
decompression was primarily indicated in the event of
localized hematomas in infarcted noneloquent brain parenchyma. Internal decompression was performed under
microscopic magnification. During the operation the patients were rehydrated with isotonic crystalloids with care
taken to maintain euvolemia and a serum osmolality of
300 mOsm/L. The target hematocrit was kept at about
30% to reduce blood viscosity.6 Colloids and inotropes
were used to keep the mean arterial blood pressure level
above 90 mm Hg. Postoperative ICP monitoring was performed in all patients who underwent DS. In the event
of postoperative ICP elevation a CT scan was performed
and the indications for repeated surgery were ruled out.
Those patients who were not candidates for repeated surgery were eligible for barbiturate coma with the aim of
achieving electroencephalographic burst suppression.

Case Reports
Case 1

History, Examination, and Diagnosis. This 32-yearold right-handed woman was transferred to our institution
from another hospital where she had presented in deep
coma after a 12-hour history of headache. At examination, the patient was comatose with no motor response to
pain and bilaterally fixed and maximally dilated pupils.
A CT scan of the brain revealed a hemorrhagic infarct
of the temporal lobe on the right side, brain edema, and
brainstem compression (Figs. 1A and B). A CT angiography study demonstrated nonvisualization of the transverse and sigmoid sinuses on the right side (Fig. 1C, D,
and E). Intravenous mannitol and hyperventilation were
ineffective.
Operation and Postoperative Course. Emergency
decompressive surgery was planned, and a large frontotemporoparietal hemicraniectomy was performed. The
sylvian veins were congested and the vein of Labbé appeared thrombotic. An intraparenchymal superficial clot
was removed, while the infarcted cerebral tissue was only
partially resected with the rationale of sparing edematous,
potentially still viable brain. At the end of the operation
the brain appeared slack, well perfused, and pulsating,
and the ICP was 5 mm Hg. The postoperative CT scan

Neurosurg. Focus / Volume 26 / June 2009

showed complete clot removal and reduction of the midline shift. On Day 3, the ICP increased up to 25 mm Hg
and a CT scan revealed an increased mass effect due to
edema and bleeding of the infarcted temporal lobe. Hypothermia and barbiturate coma were effective in lowering the ICP to 15–18 mm Hg until Day 5, when the ICP
rose to 30 mm Hg and the right pupil became maximally
dilated and unreactive to light. The patient was returned
to the operating room, where the craniotomy was enlarged at the site of the prior parietooccipital craniotomy
and the temporal squama was extensively drilled up to
the cranial base. The bone bleeding was abnormally intense, suggesting compensatory venous drainage through
the emissary veins. The theoretical hypothesis that craniotomy may affect the osseous compensatory circuits was
not a contraindication to DS because of the multiplicity
of the emissary veins and the wide distribution of the diploic venous network.12 The drilling was extended from the
superior orbital fissure to the posterior root of the zygomatic arch with the aim of maximizing the decompression and obtaining an unobstructed view of the temporal
lobe from the lateral, basal, and medial surfaces. This
exposure was considered necessary to control possible
bleeding from the congested and hypertrophic sylvian,
temporobasal, and polar veins that were compensating
for the thrombosed vein of Labbé. The dura mater was
opened. The brain appeared diffusely swollen and the sylvian veins as well as the anterior temporal veins appeared
red and congested. The infarcted tissue of the second and
third temporal gyri was resected with extreme care taken
to preserve all the veins and spare the mesial temporal
structures that were not involved in the infarction. Once
the infarcted tissue had been resected, the temporal and
sylvian veins normalized and the brain swelling rapidly
reduced. Intraoperatively, the ambient cistern and the
brainstem appeared decompressed from the uncus. The
postoperative CT scan showed complete clot removal, decompression of the ambient cistern, and absence of midline shift (Fig. 1F and G).

Outcome. At the 6-month follow-up examination the
patient’s GOS score indicated moderate disability because of partial neglect and a mild monoparesis of the left
arm. She suffered from seizures, which were controlled
with phenobarbital.
Case 2

History, Examination, and Diagnosis. This 51-yearold left-handed man was admitted to another hospital because of headache, confusion, and mild right-sided hemiparesis. A CT scan showed an intracerebral hematoma
and brain edema of the left parietal lobe with midline
shift. He was transferred to our institution, where digital
subtraction angiography demonstrated slow circulation,
stagnation of the contrast medium in the frontoparietal
ascending veins, and no opacification of the superior
sagittal sinus, suggestive of thrombosis (Fig. 2B and C).
On Day 4, the right-sided hemiparesis worsened and a
CT scan revealed the enlargement of the hematoma and
worsening of the edema and the mass effect (Fig. 2A). Osmotics were ineffective and the following day he became
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L. A. Lanterna et al.

Fig. 2. Case 2. A: Preoperative CT revealing a hemorrhagic infarction of the left parietal lobe with brain swelling and midline
shift.    B and C: Late-phase right (B) and left (C) internal carotid artery digital subtraction angiograms in frontal projection,
demonstrating stagnation of the contrast medium in the frontoparietal ascending veins and no opacification of the superior sagittal sinus.    D: Postoperative CT scan of the brain.

comatose with an abnormal flexion response to pain and
a dilated pupil on the left side.

Operation and Postoperative Course. A large frontotemporoparietooccipital hemicraniectomy was performed. The bone bleeding was abnormally intense. The
dura mater was opened. The brain appeared swollen and
the cortical veins draining into the sagittal sinus were congested and red. The clot was evacuated together with the
bleeding, congested, infarcted tissue surrounding the hematoma. The ICP remained ≤ 15 mm Hg. On Day 7, sedation was discontinued and the patient began to respond to
commands. The postoperative CT scan showed complete
clot removal and reduction of the midline shift (Fig. 2D).

Outcome. After 3 months the bone flap was repositioned. The patient returned to his normal daily life; his
GOS score indicated good recovery and the neuropsychological evaluation was normal. He suffered from seizures,
which were controlled with carbamazepine.
Case 3

History, Examination, and Diagnosis. This 39-yearold left-handed man was admitted to the emergency department because of headache, vomiting and a reduced

level of consciousness (GCS score 12). A CT scan showed
a hemorrhagic infarct of the temporal lobe on the right
side, brain swelling, and compression of the ambient cistern (Fig. 3A). An MR imaging study demonstrated the
absence of a flow signal into the transverse and sigmoid
sinuses on the right side (Fig. 3B). Diffusion-weighted images revealed predominant cytotoxic edema. During the
next 3 hours the patient’s condition deteriorated further
and, on reevalution, he was comatose (GCS score 8) with
dilation of the pupil on the right side. After resuscitation
with tracheal intubation, artificial hyperventilation, and
mannitol, the pupillary diameter normalized.
Operation and Postoperative Course. Emergency
decompressive surgery was planned and a large frontotemporoparietal hemicraniectomy, with drilling of the
temporal bone, was performed. The temporal lobe was
swollen, pale, and nonpulsating. The vein of Labbé was
thrombosed while the sylvian and anterior temporal veins
were prominent and congested. The hemorrhagic infarct
was resected (middle and inferior temporal gyrus) with
extreme care taken to preserve all the veins and to spare
the mesial temporal structures. Postoperative CT showed
complete clot removal and reduction of the temporal lobe
swelling (Fig. 3C).

Fig. 3. Case 3. A: Preoperative CT revealing a hemorrhagic infarction of the right temporal lobe with transtentorial herniation.    B: An MR venogram showing absence of flow in the transverse sinus and Labbe vein on the right side.    C: Postoperative CT of the brain.

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Craniectomy and dural sinus thrombosis
TABLE 1: Summary of published clinical series and case-reports on decompression for CVDST*

Authors & Year
Stefini et al., 1999

Weber & Spring, 2004
Keller et al., 2005

present series

GCS
Score

Pupillary Signs

Dural Sinus

Decompression

Outcome
(GOS)

4
6
5
<8

bilaterally dilated
bilaterally dilated
bilaterally dilated
unilaterally dilated

transverse & sigmoid
transverse & sigmoid
transverse & sigmoid
transverse & sigmoid

ED
ED
ED & drainage of a superficial clot
ED

GR
GR
SD
MD

9
6
13
13
3
5
8

normal
normal
normal
normal
bilaterally dilated
unilaterally dilated
unilaterally dilated

superior sagittal
frontal cortical veins
transverse & sigmoid
transverse & sigmoid
transverse & sigmoid
superior sagittal
transverse & sigmoid

ED & ID
ED & ID
ED & ID
ED
ED & ID
&
ED and ID

GR
GR
MD
MD
MD
GR
GR

* Based on MEDLINE and EMBASE search from 1970 to 2008. Abbreviations: ED = external decompression (defined as craniectomy and duraplasty); GCS = Glasgow Coma Scale; GOS = Glasgow Outcome Scale; GR = Good Recovery; MD = Moderate
Disability; ID = internal decompression (defined as hematoma drainage and resection of necrotic tissue); SD = Severe Disability.

Outcome. After 1 month the patient’s GOS score indicated good recovery. He did not suffer from seizures.
The neuropsychological assessment was normal.

Discussion

The clinical history of these 3 patients supports the
hypothesis that emergency DS may be life-saving in patients with transtentorial herniation due to CVDST and
that both the functional and the neuropsychological outcome may be favorable, even in deeply comatose patients
with ominous pupillary signs. No intracranial bleeding
complications directly related to the DS occurred and no
patient developed postoperative hydrocephalus.
Consistent with the rarity of the pathology, a MEDLINE and EMBASE search of the literature from January
1970 to October 2008 using 6 key words (cerebral, dural
sinus, vein, thrombosis, surgery, decompression) revealed
only 3 surgical reports on patients (a total of 8) who underwent DS for CVDST.11,17,20 Four of these 8 patients had
pupillary signs of brain herniation17,20 (Table 1).
Our unexpectedly favorable results were consistent
with those reported in the literature. Including our 3 patients, 6 of the 7 patients who were moribund with pupillary signs were independent in daily living after discharge
from the rehabilitation units.17,20 Furthermore, Keller and
colleagues11 observed a good functional outcome (moderate disability, 2 cases; good recovery, 2 cases) in all 4 of
their patients who underwent DS before developing clinical signs of herniation (Table 1). The 2 patients who were
categorized as having moderate disability suffered from
slight focal signs probably related to the eloquence of the
cortex involved in the hemorrhagic infarction.11
Although the analysis of case reports and small case
series may be affected by publication bias and a formal
statistical investigation of confounding variables and
procedure-related risk factors is impossible, the reported
clinical results are worthy of attention for at least 2 reasons: 1) according to the ISCVT analyses, all patients had
Neurosurg. Focus / Volume 26 / June 2009

one or more of the main independent predictors of death
(intracranial hemorrhage, clinical worsening, GCS score
< 9, new focal sign);7 and 2) the most frequent CVDST
mechanism of death is transtentorial herniation, and 7 of
the 11 patients already had related clinical signs.2
Explanations of how DS may affect the physiopathology of CVDST can only be speculative. Cerebral venous
and dural sinus thrombosis causes a wide spectrum of
parenchymal changes, ranging from vasogenic and cytotoxic edema to intracerebral hematomas.3,5 These complications may lead to a compartmentalized intracranial
hypertension that secondarily compresses intraparenchymal veins, with a subsequent worsening of edema and
swelling. Furthermore, in CVDST the regional cerebral
blood flow may be reduced because of paradoxical arteriolar vasoconstriction.5,19 A condition that, based on
experimental data, has features reminiscent of ischemic
penumbra.18 Decompressive surgery creates space for the
swelling brain and, by reducing intracranial hypertension
and brainstem compression, may break the vicious cycle
by relieving arteriolar constriction and restoring flow in
compressed venous collaterals.
In view of the rarity of patients with malignant
CVDSTs necessitating emergency DS, the surgical experience is limited and accepted guidelines on how to perform the decompression are lacking. The review shows
that there is no unanimity as to what constitutes the preferable surgical strategy. Different authors have adopted
distinct approaches: pure external decompression (in 5
cases) or internal decompression with or without removal
of the bone flap (in 6 cases) (Table 1). A statistical comparison of the results obtained with the 2 strategies is beyond the limits of small series because of limited power
and clinical, timing, and risk-factor heterogeneity among
the studies.
In our experience, we tried to define criteria a priori
to guide surgical decision making. In particular, we considered the site and characteristics of the clot and the eloquence of the brain, with the aim of tailoring surgery and
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L. A. Lanterna et al.
reducing its burden in a situation where cytotoxic edema
may coexist with viable brain.5,13 In practice, the peculiarities of the cerebral lesions (for example, site, clot dimension, depth), together with the clinical course and the
supposed hemispheric dominance, guided our decisions
toward internal decompression with removal of the bone
flap in all cases. In the light of the favorable neuropsychological outcomes, this experience appears reasonable and
is in accordance with that of other authors.11
On the other hand, other case reports have shown almost equally favorable results with pure external decompressions.17,20 Recently, MR imaging studies have demonstrated the existence of parenchymal changes (vasogenic
edema) that could be completely reversible, and such studies may be advocated in support of a less invasive surgical approach.16 From the analysis of the cases in which
patients were treated by means of external decompression, the importance of surgical timing emerges. Stefini et
al.17 observed that the ICP can be better controlled when
the operation is promptly performed. The importance of
timing may be indirectly supported by the recent trials
investigating external decompression for patients with
space-occupying arterial infarcts.10
In conclusion, although the rarity of the condition
precludes any statistically based evidence, the functional
recovery obtained in a situation in which the prognosis
would otherwise have been grim15 appears clinically relevant. Decompressive surgery may offer the last chance
of life and a favorable functional outcome in selected patients with CVDST whose condition is deteriorating because of impending brain herniation that is unresponsive
to causal therapy and intensive care. In the future, updates
on the pathophysiology of CVDST and new developments
in imaging technologies will provide a better and more
comprehensive insight into the specific therapeutic requirements of each patient. A patient-specific pathophysiologically based approach could enable the clinician to
choose the appropriate surgical strategy and timing with
more accuracy and, probably, greater effectiveness.
Disclosure
The authors report no conflict of interest concerning the material or methods used in this study or the findings specified in this
paper.
Acknowledgments
The authors thank Mario Lanterna and Alida Scolari for their
invaluable advice.
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Manuscript submitted January 10, 2009.
Accepted March 30, 2009.
Portions of this work were presented in poster form at the
57th Italian Conference of Neurosurgery, Udine, Italy, November
8, 2008.
Address correspondence to: Luigi A. Lanterna, M.D., Ph.D., Via
B Crespi, 13 Milano, Italy. email: l.lanterna@virgilio.it.

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