Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70

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Interdisciplinary Neurosurgery: Advanced Techniques and

Case Management
journal homepage: www.inat-journal.com

Neuroanatomical Study

Lateral sinus thrombosis following minor head injury in children

Jun Maruya a,⁎, Satoshi Tamura a, Takaharu Miyauchi b, Keiichi Nishimaki a
a
Department of Neurosurgery, Akita Red Cross Hospital, Japan
b
Department of Radiology, Akita Red Cross Hospital, Japan

a r t i c l e i n f o a b s t r a c t

Article history: Objective: In children, lateral sinus thrombosis (LST) following minor head injury (MHI) has occasionally been re-
Received 21 November 2016 ported because of neuroimaging techniques. However, the condition is rare, and its pathophysiology remains un-
Revised 26 November 2016 known. We aimed to identify the factors associated with its etiology and severity to provide information to guide
Accepted 4 December 2016 the diagnosis, management, and prognosis.
Methods: We retrospectively reviewed all patients aged 1–15 years with craniofacial trauma presenting to our
Keywords:
emergency department between 2011 and 2015. In total, 4 patients with LST following MHI were identified.
Lateral sinus thrombosis
Sigmoid sinus thrombosis
We also performed a comprehensive literature review to identify relevant cases in studies published between
Transverse sinus thrombosis 1990 and 2015, and this yielded 17 studies with 24 patients. We analyzed the data for these 24 patients with
Mild head injury our 4 cases (n = 28).
Child Results: The mean age of the 28 cases was 7.0 years, and the male-to-female ratio was 1.2:1. Nausea/vomiting and
Anticoagulation headache were the most common symptoms, but signs and symptoms of increased intracranial pressure were
present in 5 patients. The sigmoid sinus was most commonly affected. A total of 20 patients were treated conser-
vatively, and the remaining 8 patients received anticoagulation. All patients had good outcomes, with no major
complications. Radiological follow up showed complete recanalization in 14 patients and partial recanalization in
3 patients.
Conclusions: Although LST following MHI is still rare in children, our findings indicate that it might be much more
common than previously thought. Thankfully, though, most patients appear to have an excellent prognosis. A
high degree of suspicion should be maintained when assessing patients with MHI, because the non-specific
symptoms make diagnosis difficult. Neuroimaging by magnetic resonance venography or computed tomography
venography is crucial for both diagnosis and follow up. Hypercoagulation disorders should be excluded, and
anticoagulation therapy should be given to patients with these disorders, or to those with persistent or progres-
sive LST. Conservative therapy is recommended, although anti-edema drugs or intermittent lumbar puncture
may be beneficial.
© 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/).

1. Introduction The safety of anticoagulation therapy has been established in pediat-

Lateral sinus thrombosis (LST) in children has mostly been reported
as a complication of otitis media [1,2]. However, since the antibiotic era
there has been a dramatic reduction in intracranial complications from
infectious ear disease [2,3]. Thus, although it can still complicate
minor head injury (MHI), LST is now rare in childhood [4]. Whereas
the history and clinical presentation are more likely to lead to a diagno-
sis of LST in adults, the clinical signs and symptoms are less specific in
children [1,5]. Therefore, the diagnosis of pediatric LST following MHI
is not easy [6]. Early diagnosis has latterly become possible courtesy of
the widespread use of neuroimaging, with occasional cases of pediatric
LST following MHI being reported in the literature [3,4,6–20]. However,
the pathophysiology of this rare complication is still unknown.
⁎ Corresponding author at: Department of Neurosurgery, Akita Red Cross Hospital, 222-
1 Nawashirosawa, Saruta, Kamikitate, Akita 010-1495, Japan.
E-mail address: jmaruya@archosp-1998.com (J. Maruya).
ric cases of cerebral sinus thrombosis [21,22]. But, intracranial hemor-
rhage frequently occurs in pediatric cases of cerebral sinus thrombosis
following head injury, so anticoagulation therapy is often withheld.
The role of anticoagulation therapy is therefore still controversial in
these cases [4], and management decisions are left to the preference
of the treating physician.
We performed a literature review to identify cases of pediatric LST
following MHI. This review aimed to identify the factors associated
with the etiology and severity of pediatric LST following MHI. Ultimate-
ly, we discuss how these can guide the diagnosis, management, and
prognosis of this rare entity.
2. Patients and methods
Pediatric LST following MHI was defined as radiologically confirmed
LST following a documented MHI in a child aged 1 to 15 years. A child

http://dx.doi.org/10.1016/j.inat.2016.12.002
2214-7519/© 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
 J. Maruya et al. / Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70
was determined as having sustained an MHI based on an appropriate
history of head trauma and an admission Glasgow Coma Scale (GCS)
score of 13–15. We retrospectively reviewed all pediatric patients
aged 1–15 years presenting to our emergency department with cranio-
facial trauma between January 2011 and December 2015, inclusive.
From among these 1202 patients, we identified 4 who met the inclusion
criteria. We then retrospectively analyzed their clinical records and ra-
diological findings.
Next, we performed a comprehensive literature review to identify
relevant studies published between 1990 and 2015 in PubMed, Google
Scholar, and Ichushi-Web (for articles written in Japanese). The search
terms were as follows: “lateral sinus thrombosis,” “transverse sinus
thrombosis,” “sigmoid sinus thrombosis,” “childhood,” “children,”
“minor head trauma,” and “minor head injury.” The reference lists of rel-
evant publications were also reviewed to identify additional papers that
might have been missed by our search terms. We included those papers
in which a GCS score had not been mentioned, children did not have ob-
vious disturbance of consciousness, or children were diagnosed as hav-
ing MHI by the authors. We identified 17 related studies that included
medical data for 24 patients.
The data for the 24 patients identified in the literature review were
merged with those of our 4 cases, and we analyzed the clinical features,
risk factors, follow up, outcomes, and management. We also provide an
illustrative case.
3. Results
3.1. An illustrative case
A 7-year-old boy fell off his bike and struck his occiput. He returned
home unaided and able to ride his bike; however, he seemed sleepier
than normal and complained of a headache, so was taken to the emer-
gency room approximately 3 h after the fall. On initial evaluation, he
had stable vital signs, no neurological deficits, and a GCS score of 15. A
computed tomography (CT) scan was done following an episode of
vomiting in the emergency room, and this demonstrated a very small
acute epidural hematoma at the left cerebellar convexity. He was
allowed to go home, but neurosurgical follow up was arranged early
the following morning. On return, his neurological examination was un-
remarkable, but a repeat CT scan revealed that he had developed a focal
hyperdensity in the left sigmoid sinus (Fig. 1A) and that the acute epi-
dural hematoma had enlarged (Fig. 1B). Meticulous reading of bone
window imaging indicated a left lambdoid suture diastasis (Fig. 1C).
Subsequently, magnetic resonance (MR) imaging with MR venography
was performed, which confirmed that the acute epidural hematoma
had not changed in size. Both the T1- and T2-weighted MR images
showed an area of isointensity in the left sigmoid sinus that was sugges-
tive of an LST (Fig. 2). There were no other intracranial lesions. MR
venography confirmed occlusion of the left transverse and sigmoid
sinus, with the development of venous collaterals around the superficial
middle cerebral vein (Fig. 3A). The child was managed conservatively,
and he made a full recovery. He was discharged home 7 days after the
initial trauma, and follow-up MR venography after 2 months showed
recanalization of the transverse and sigmoid sinuses (Fig. 3B).
3.2. Literature review
Including our 4 cases, there were 28 reports of pediatric patients
with LST following MHI (Table 1). The age range of patients was from
1 to 15 years (mean age 7.0), and there were 15 males and 13 females
(male-to-female ratio of 1.2:1). The mechanism of injury was either a
fall or a motor vehicle accident. The time from head trauma to admis-
sion typically varied from immediately post-trauma to 2 days after the
trauma. However, this was not universal, with case 12 being admitted
on day 4 and case 24 being admitted on day 5 because of delayed diag-
nosis and minimal symptoms, respectively. In addition, due to
65
exacerbation after temporary remission, cases 13 and 14 were
readmitted on days 10 and 6, respectively. On laboratory investigation,
only case 13 had hematological evidence of a prothrombotic disorder
(elevated antiphospholipid antibodies).
Data on the clinical symptoms and signs were available for 23 pa-
tients (Table 2). Commonly reported clinical findings included nausea
and/or vomiting (23 cases, 100%), headache (16 cases, 69.6%), gait ataxia
(5 cases, 21.7%), drowsiness (4 cases, 17.4%), papilledema (4 cases,
17.4%), irritability (4 cases, 17.4%), dizziness, and imbalance (3 cases,
13.0%). In 2 cases each (8.7%), there was evidence of abducens palsy or
diplopia, photophobia, hearing disturbance, raccoon eyes (periorbital ec-
chymosis), Battle's sign (mastoid ecchymosis), or hemotympanum. In
addition, 1 patient each (4.3%) had blurred vision, amnesia, nystagmus,
otorrhea, pyrexia, or decreased muscle tone. Finally, 5 patients had
signs or symptoms of increased intracranial pressure (IICP), including
papilledema, abducens palsy, drowsiness, and high opening pressure at
lumbar puncture (Table 3). Although the initial symptoms were typically
non-specific, some patients did therefore present with diagnostic signs
of IICP; these were early symptoms in 2 patients (cases 10 and 17), but
were delayed symptoms in 3 patients (cases 12, 13, 23).
Radiological evaluation revealed skull fractures in 18 children
(64.3%; vault = 15, base = 5, and diaschisis of lambdoid suture = 5).
Pneumocephalus was detected in 8 patients (28.6%), and intracranial
hematomas were recognized in 14 patients (50.0%; acute epidural he-
matoma = 8, acute subdural hematoma = 6, and cerebral contusion =
4). Hematoma expansion did not occur in all patients regardless of the
treatment strategy used. Five children (17.9%) had neither skull frac-
tures nor intracranial hematomas. The diagnosis of LST was established
by contrast-enhanced CT, MR venography, or CT venography. A single
sinus was involved in 13 patients (46.4%), with the transverse sinus in-
volved in 4 cases and the sigmoid sinus in 9 cases. But, there was multi-
ple sinus involvement in 15 patients (53.6%), including the transverse
and sigmoid sinuses in 9 cases, the sigmoid sinus and jugular vein in 4
cases, and the transverse-sigmoid sinus and jugular vein in 2 cases.
Conservative therapy was sufficient in 20 patients (71.4%), but 8 pa-
tients (28.6%) were treated with anticoagulation therapy (heparin, low
molecular weight heparin [LMWH], enoxaparin, warfarin, and/or
acenocoumarol). Radiological follow up showed complete and partial
recanalization in 14 (duration range: a couple of days to 2 months)
and 3 patients (3 days to 5 months), respectively. The median follow-
up period was 2 months, with a range from 18 days to 8 months. The
outcome was good in all patients, with no major complications report-
ed. However, 2 patients (cases 5 and 9) were still suffering from recur-
rent headaches for a couple of months.
4. Discussion
4.1. Etiology
LST has been attributed to several etiologies, including: 1) infection
(e.g., acute or chronic otitis media), 2) systemic conditions (e.g., coagu-
lation disorders, such as protein C and S deficiency or thrombophilias
such as antiphospholipid syndrome and metastatic malignancy), 3)
drug induced conditions (e.g., cytotoxic drugs, contraceptive pills, or
hormone replace therapy), and 4) trauma (e.g., penetrating severe
head injury, closed head injury, or posterior fossa surgery) [1,4,10,23].
Given that LST from infective causes has become a rare presentation in
children since the advent of antibiotics [2,3], trauma and hypercoagula-
ble states have emerged as equally significant causes [3]. Outside the
neonatal period, the incidence of cerebral sinus thrombosis has been re-
ported to be 0.34 per 100,000 per year [15,20], but the incidence of pe-
diatric LST following MHI is unknown. In our experience, we identified 4
children with LST from 1202 pediatric patients with craniofacial trauma
over a 5-year period, and we did not identify any other brain regions
with cerebral sinus thrombosis. This is consistent with reports that
LST is the most frequent type of cerebral sinus thrombosis, especially
66 J. Maruya et al. / Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70

A B

C
Fig. 1. Axial non-contrast computed tomography scans revealing a focal hyperdensity of the left sigmoid sinus (dense sigmoid sinus sign) (A) and the acute epidural hematoma (B, arrow).
Meticulous reading of the bone window imaging demonstrates left lambdoid suture diastasis (C, arrowhead).

following pediatric MHI [15,20,24], and with reports that the superior pediatric LST following MHI might not be as rare as we previously
sagittal sinus and deep venous system are rarely obstructed after MHI thought, considering the fact that we cannot exclude the possibility of
[24]. Nevertheless, our experience also suggests that the incidence of diagnosis being missed because of mild or non-specific symptoms.

Fig. 2. T1-weighted magnetic resonance imaging showing an isointensity area in the left sigmoid sinus (A), and T2-weighted magnetic resonance imaging also demonstrating an
isointensity area in the left sigmoid sinus (B). Parenchymal lesions are not detected except for the acute epidural hematoma.
 J. Maruya et al. / Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70
Fig. 3. Initial magnetic resonance venography showing a complete thrombosis in the left
transverse and sigmoid sinus (A). Follow-up magnetic resonance venography after two
months demonstrating a recanalization (B).
4.2. Mechanism
Although several theories have been suggested, the exact mecha-
nism of cerebral sinus thrombosis following closed head injury is still
unclear [4,10,25]. When a fracture is the cause, cerebral sinus thrombo-
sis is commonly attributed to the linear fracture crossing the wall of the
dural sinus [10,12,26]. A direct compression of the sinus by adjacent
structures, such as a pneumocephalus or an epidural hematoma, can in-
duce progressive thrombosis [4]. Equally, sinus wall trauma with intra-
mural hemorrhage or injury to the lining epithelium can cause sinus
thrombosis [4,10]. Finally, inward extension of a thrombus from an in-
jured emissary vein can completely block the sinus [4,10].
Another suggested mechanism is the blood coagulation cascade trig-
gered by closed head injury. Disrupted coagulation, disturbances in
blood flow (venous stasis), or capillary damage may each predispose a
person to thrombosis [24,25]. The lateral sinus follows an s-shaped
course in the posterior cranial fossa, forming grooves in the petrous,
temporal, and occipital bones. Given that the lateral sinuses are only
lined with endothelium, they have no muscle, and their bases are
formed on bone, they are very vulnerable to shear force injury [24].
Compared with adults, pediatric patients tend to be affected more
often by traumatic cerebral sinus thrombosis because of the immaturity
of their cerebral venous collateral vasculature [24].
4.3. Signs and symptoms
Pediatric LST following MHI may present anywhere from immediately
after to several days after the injury. Although the symptoms were highly
67
non-specific in the analyzed cases, they could be broadly categorized into
four groups: 1) symptoms of cerebral concussion, such as headache, nau-
sea, irritability, amnesia; 2) symptoms of labyrinthine concussion, such as
nausea, ataxia, dizziness, nystagmus, gait imbalance, and hearing distur-
bance; 3) symptoms of IICP, such as headache, vomiting, papilledema,
abducens palsy, drowsiness, and blurred vision; and 4) other symptoms
such as raccoon eyes, Battle's sign, hemotympanum, and otorrhea.
Headache and nausea/vomiting were the most commonly reported
symptoms among the cases reviewed, consistent with that expected fol-
lowing a pediatric MHI, and probably due to either cerebral concussion or
IICP. Therefore, there is a need to be careful when making a differential
diagnosis based on these symptoms. Checking for papilledema or high
opening pressure at lumbar puncture can be helpful in the recognition
of IICP, and should certainly be performed in the case of worsening symp-
toms or symptoms that persist over a period of several days. If exacerba-
tion of headache and vomiting occurs after temporary remission, careful
evaluation is needed to avoid the risk of misdiagnosing IICP. A girl in our
review (case 14) was first diagnosed with acute viral gastroenteritis, and
we speculate that her persistent nausea and vomiting must have been
caused by IICP, though a detailed description of her clinical signs and
symptoms was not available [11]. No cases of focal neurological deficit,
such as convulsive seizure and hemiparesis, due to venous infarction
were indicated in the included cases, whereas focal syndrome or enceph-
alopathy has been reported in 31% of adult patients with isolated LST [2].
4.4. Diagnosis
The diagnosis of pediatric LST following MHI is difficult, not only be-
cause of the rarity of the disorder but also because of the non-specific
symptoms. Therefore, a high degree of suspicion should be maintained
early in the presentation of patients with certain signs or symptoms to
ensure correct and timely diagnosis [4,15]. An MHI that is followed by
a progressively worsening headache, vomiting, or imbalance, with or
without visual disturbance, should lead the clinician to be suspicious
of a traumatic LST, even when presentation is up to several days after
the injury [6]. Neuroimaging is crucial for both diagnosis and follow
up in these cases [22]. If a skull fracture is noted to cross a lateral sinus
on radiography and/or CT, further radiological examination should be
considered [7]. Sometimes pediatric LST following MHI can be identified
on non-contrast CT, as clots in the sigmoid sinus, by the “dense sigmoid
sinus sign” [6]. This sign is important for suspicious cases that do not
have evidence of either skull fracture or intracranial hematoma, because
it may trigger the suspicion of LST. Actually, no specific symptoms or
signs were recognized in five children who had neither skull fractures
nor intracranial hematomas in our review, however “dens sigmoid
sinus sign” was identified in all five cases and it was the only trigger
for the diagnosis of LST. Confirmation of diagnosis relies on demonstrat-
ing LST by either MR venography or CT venography, though the former
of these is the most sensitive imaging tool and can provide direct nonin-
vasive visualization of the dural sinuses and abnormalities in sinus flow
[27]. Cerebral and cerebellar parenchymal lesions can also be assessed
with better sensitivity [4]. However, CT venography does have some ad-
vantages over MR imaging, because it allows precise and rapid assess-
ment of fractures, often without the need for sedation [4].
4.5. Management
LST following MHI resolves spontaneously in most patients, so
would not require anticoagulation. But we must consider that LST can
lead to catastrophic outcomes, such as a large venous infarction, and
that some patients present with persistent symptoms or evidence of
IICP. Although such cases might require anticoagulation therapy [10,
11,13,19], the role of such therapy is still highly controversial in trau-
matic cerebral sinus thrombosis. Because there are so few case reports
of patients with cerebral sinus thrombosis following MHI, no definitive
answer has been provided as to which therapy is best [4].
68 J. Maruya et al. / Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70

Table 1
Clinical features of reported cases of lateral sinus thrombosis following mild head injury in the pediatric population.

Authors Skull Intracranial Thrombosis Time to Time to

Case No Age / Sex Treatment Follow-up period Outcome
(year) fracture lesion extension admission recanalization
1 Taha (1993) 7/M V, B P Lt SS - JV N.A. Conservative N.A. N.A. Normal

2 6/M (-) (-) Lt SS - JV N.A. Conservative N.A. N.A. Normal

3 4/M (-) (-) Lt SS N.A. Conservative N.A. N.A. Normal

4 1/F V P Lt SS N.A. Conservative N.A. N.A. Normal

5 Stiefel (2000) 13 / F V, DLS AEH Lt TS N.A. Conservative Complete / 2 Mo 2 Mo Headache

6 9/F V, B, DLS C, ASH Rt TS N.A. Conservative Complete / 6 W 6W Normal

7 9/F V, B (-) Rt SS N.A. Conservative Partial / 5 Mo 5 Mo Normal

8 2/M V, DLS (-) Rt TS - SS N.A. Conservative Complete / 2 Mo 2 Mo Normal

9 15 / F B (-) Rt TS N.A. Conservative N.A. 3 Mo Headache

10 Satoh (2000) 1/M N.A. AEH Lt SS Day 1 Conservative Complete / 15 D 3.5 Mo Normal

11 Sousa (2004) 7/F (-) (-) Rt SS Day 0 Conservative N.A. 1 Mo Normal

12 Nelson (2004) 4/F (-) ASH Rt TS - SS Day 4 Conservative Complete / 6 W 6W Normal

13 Muthukumar (2005) 7/F V (-) Rt TS Day 10* Acenocoumarol N.A. 3W Normal

14 Saad (2005) 10 / F (-) (-) Rt TS - SS Day 6* Hep → Enoxaparin N.A. 6 Mo Normal

15 Yuen (2005) 4/F (-) (-) Rt TS - SS Day 0 Conservative Complete / 10 W 10 W Normal

16 Nehme (2009) 7/M (-) P, AEH Rt TS - SS Day 2 Conservative Partial / 2 Mo 4 Mo Normal

17 Lakhkar (2010) 9/M DLS (-) Rt TS - SS Day 1 Hep → Warfarin N.A. N.A. Normal

18 Fujita (2010) 6/M V ASH Rt TS - SS Day 0 Conservative Complete / 15 D 18 D Normal

19 Pikis (2013) 3/F V (-) Lt SS Day 0 Enoxaparin Complete / 1 Mo 1 Mo Normal

20 Georgoulis (2014) 6/F V C, ASH Rt TS - JV Day 0 Hep → Warfarin N.A. 6 Mo Normal

21 Lebowitz (2014) 6/M N.A. ASH Lt TS - JV Day 0 Enoxaparin N.A. 3 Mo Normal

22 Award (2014) 12 / M V P Rt SS - JV Day 0 Hep → Enoxaparin Partial / 3 D 7W Normal

23 Rajz (2014) 9/M N.A. AEH Rt SS Day 1 Hep → LMWH Complete / 1 W N.A. Normal

24 Yun (2015) 10 / M V P, AEH Rt SS Day 5 Conservative Complete / 3 W 3W Normal

25 Our cases 7/M DLS AEH Lt TS - SS Day 1 Conservative Complete / 2 Mo 6W Normal

26 6/M V P, C, ASH Rt TS - SS Day 0 Conservative Complete / 2 Mo 10 W Normal

27 7/M V P, AEH Rt SS Day 1 Conservative Complete / 1 Mo 6W Normal

28 8/F V, B P, C, AEH Lt SS - JV Day 0 Conservative Complete / 1 Mo 8 Mo Normal

⁎ Readmission. M = male, F = female, V = vault, B = base, DLS = diaschisis of lambdoid suture, P = pneumocephalus, C = contusion, ASH = acute subdurala hematoma, AEP = acute
epidural hematoma, Rt = right, Lt = left, TS = transverse sinus, SS = sigmoid sinus, JV = jugular vein, Hep = heparin, LMWH = low molecular wight heparin, D = day, W = week, Mo =
month, POD = postoperative day, N.A. = not available. Shaded row represents a case with symptoms related to increased intracranial pressure.

Some authors suggest that systemic anticoagulation therapy is
safe and effective in limiting clot propagation, and that its use
could facilitate more rapid recanalization [4]. Supporting the safety
of this approach, none of the cases who received anticoagulation
therapy in our review developed new neurological symptoms or
other complications. However, the increased risk for venous hemor-
rhagic infarction must be considered [27], requiring that pediatric
patients be monitored carefully [20]. Based on this, and to address
concerns about causing hemorrhages to progress aggressively,
some authors recommended using LMWH instead of heparin
when treating cerebral sinus thrombosis with intracranial hemor-
rhage [22]. Many authors, though, do not advocate prophylactic
anticoagulation therapy, and instead suggest that anticoagulation
therapy should be reserved for clinical deterioration [1,6,7,12] (e.g.,
these cases were managed conservatively to avoid secondary intra-
cranial hemorrhage, and recovery was uneventful).
Finally, anti-edema drugs might be useful for controlling IICP in
traumatic cerebral sinus thrombosis, with agents such as mannitol,
glycerol, or corticosteroid all being suitable, as well as intermittent
lumbar puncture [8,28,29]. Overall, we suggest the following protocol
for the management of pediatric LST following MHI:
1) Hypercoagulation disorders should be excluded, including those
caused by otitis media, protein S or C deficiency, antiphospholipid
syndrome, malignancy, contraceptive drugs, and hormone replace-
ment therapy. Systemic anticoagulation therapy with LMWH should
be considered if these conditions are present.
2) Patients without hypercoagulation disorders should initially be
treated conservatively, ensuring sufficient hydration and close neu-
rological observation.
 J. Maruya et al. / Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70 69

Table 2 and the extent of thrombosis, the route of occlusion, the collateral
Signs and symptoms in pediatric patients with lateral sinus thrombosis following mild circulation, the age of the patient, and the nature of any underlying
head injury.
disease [4]. Nevertheless, especially in pediatric LST following MHI,
Symptom No. of patients, n = 23 (%) patients appear to have an excellent prognosis regardless of the
Nausea / Vomiting 23 (100)
treatment strategy used.
Non-dominant sigmoid sinus thrombosis rarely produces any
Headache 16 (69.6)
neurological deficit and is associated with a good outcome [12].
Gait ataxia 5 (21.7)
When a thrombosis affects the vein of Labbé, an ischemic or hemor-
Drowsiness 4 (17.4) rhagic lesion may develop with subsequent focal signs in adults ac-
Papilledema 4 (17.4) companied by various hypercoagulation disorders [2], whereas
Irritability 4 (17.4) thrombosis is restricted to the lateral sinus in children following
Dizziness / Imbalance 3 (13.0) MHI; indeed, focal signs are usually absent, and the usual pattern is
of isolated IICP [4]. In the case of a hypoplastic contralateral lateral
Abducens palsy / Diplopia 2 (8.7)
sinus, or extension of the thrombosis from the lateral sinus to the
Photophobia 2 (8.7)
straight sinus or superior sagittal sinus, close observation should be
Hearing disturbance 2 (8.7) maintained for signs of IICP. Risk factors associated with pediatric ce-
Raccoon eyes 2 (8.7) rebral sinus thrombosis after MHI include gastroenteritis, protein S
Battle's sign 2 (8.7) deficiency, antiphospholipid antibodies, estroprogestenic medica-
Hemotympanum 2 (8.7) tions, and malnutrition [15].
Recanalization of most thrombosed sinuses can be expected
Blurred vision 1 (4.3)
to occur within 4–6 weeks after the injury [3]. However, early spon-
Amnesia 1 (4.3)
taneous recanalization occurred in cases 10, 18, and 24 in this study,
Nystagumus 1 (4.3) which may be because of greater fibrinolytic activity than
Otorrhea 1 (4.3) procoagulation activity [20]. The regression of acute deep vein
Pyrexia 1 (4.3) thrombosis begins early and is accompanied by a significant in-
Decreased muscle tone 1 (4.3) crease in tissue plasminogen activator, an endogenous fibrinolytic
Shaded row indicates a symptom recognized in the cases associated with increased agent [30]. The reason for excellent prognosis of pediatric LST fol-
intracranial pressure. lowing MHI is not clear, however we speculate that progression of
thromobosis may be mild and rapid thrombolysis may occur in
such children without hypercoagulation disorders. It is possible
that the early regression of pediatric LST following MHI might not
3) Follow-up radiological examination (MR venography or CT venogra- only be responsible for the excellent prognosis but might also ac-
phy) should be performed if patients meet at least one of the follow- count for the misdiagnosis that occurs by promoting spontaneous
ing criteria: regression and an uneventful recovery [20].
a) Worsening of symptoms
b) Persistent symptoms over a period of several days
c) Episode of IICP 5. Conclusion

4) If patients meet at least one of the above criteria, although regression
of LST is observed on follow-up radiological examination, intermit-
tent lumbar puncture or anti-edema drugs, such as mannitol, glycer-
ol, or corticosteroids, may be beneficial.
5) If patients meet at least one of the above criteria, and LST seems
mostly unchanged or progression of LST is recognized on follow-up
radiological examination, systemic anticoagulation therapy with
LMWH may be considered reasonable.
4.6. Prognosis
The clinical course of traumatic cerebral sinus thrombosis is un-
predictable, and it can vary from an asymptomatic to a fatal course.
This variability is dependent on many factors, including the site
LST following MHI was shown to occur rarely in children,
though it might actually be much more common than previously
thought, and it appears that most patients have an excellent prog-
nosis. The diagnosis is especially difficult because of its rarity and
the non-specific symptoms, so it is essential that clinicians main-
tain a high degree of suspicion when managing MHI. Neuroimag-
ing, including MR venography and CT venography, is crucial for
both diagnosis and follow up assessments. Hypercoagulation disor-
ders need to be ruled out, and when present, anticoagulation ther-
apy with LMWH should be given. Anticoagulation therapy may also
be given for patients with persistent or progressive LST. But conser-
vative therapy with sufficient hydration is recommended for most
cases, although anti-edema drugs or intermittent lumbar puncture
may be beneficial.

Table 3
Clinical features of cases with signs and symptoms related to increased intracranial pressure in pediatric patients with lateral sinus thrombosis following mild head injury.

Case Time to presentation of IICP

No Initial symptoms Diagnostic signs of IICP sign Risk factors

10 Headache, vomiting, gait ataxia, decreased Lumbar puncture: 240 mm H2O Day 1
muscle tone
12 Headache, vomiting Papilledema Day 4
13 Headache, vomiting Abducens palsy, papilledema Day 10 Hypoplastic contralateral TS, antiphospholipid
antibody
17 Headache, vomiting Papilledema, drowsiness Day 1
23 Headache, vomiting, photophobia Abducens palsy, papilledema, blurred Day 3 Hypoplastic contralateral TS
vision

IICP = increased intracranial pressure, TS = transverse sinus.

70 J. Maruya et al. / Interdisciplinary Neurosurgery: Advanced Techniques and Case Management 7 (2017) 64–70
References
[1] D. Holzmann, T.A. Huisman, T.E. Linder, Lateral dural sinus thrombosis in childhood,
Laryngoscope 109 (1999) 645–651.
[2] M. Damak, I. Crassard, V. Wolff, M.G. Bousser, Isolated lateral sinus thrombosis: a se-
ries of 62 patients, Stroke 40 (2009) 476–481.
[3] K. Nelson, K. Ward, A.S. Narang, Posttraumatic pseudotumor cerebri in a 4-year-old
female, Pediatr. Emerg. Care 20 (2004) 460–463.
[4] J. Nehme, J.C. Décarie, I. Saliba, Lateral sinus thrombosis: complication of minor head
injury, Int. J. Pediatr. Otorhinolaryngol. 73 (2009) 629–635.
[5] G. Sébire, B. Tabarki, D.E. Saunders, I. Leroy, R. Liesner, C. Saint-Martin, B. Husson,
A.N. Williams, A. Wade, F.J. Kirkham, Cerebral venous sinus thrombosis in children:
risk factors, presentation, diagnosis and outcome, Brain 128 (2005) 477–489.
[6] J.M. Taha, K.R. Crone, T.S. Berger, W.W. Becket, E.C. Prenger, Sigmoid sinus thrombo-
sis after closed head injury in children, Neurosurgery 32 (1993) 541–545.
[7] D. Stiefel, G. Eich, P. Sacher, Posttraumatic dural sinus thrombosis in children, Eur. J.
Pediatr. Surg. 10 (2000) 41–44.
[8] H. Satoh, K. Kumano, R. Ogami, T. Nishi, J. Onda, S. Nishimura, K. Kurisu, Sigmoid
sinus thrombosis after mild closed head injury in an infant: diagnosis by magnetic
resonance imaging in the acute phase–case report, Neurol. Med. Chir. (Tokyo) 40
(2000) 361–365.
[9] J. Sousa, D. O'Brien, R. Bartlett, J. Vaz, Sigmoid sinus thrombosis in a child after closed
head injury, Br. J. Neurosurg. 18 (2004) 187–188.
[10] N. Muthukumar, Uncommon cause of sinus thrombosis following closed mild head
injury in a child, Childs Nerv. Syst. 21 (2005) 86–88.
[11] D.F. Saad, G.I. Crawford, M.L. Wulkan, Cerebral venous thrombosis after closed head
injury in a child, J. Trauma 58 (2005) 1066–1067.
[12] H.W. Yuen, B.K. Gan, W.T. Seow, H.K. Tan, Dural sinus thrombosis after minor head
injury in a child, Ann. Acad. Med. Singap. 34 (2005) 639–641.
[13] B. Lakhkar, B. Lakhkar, B.R. Singh, A. Agrawal, Traumatic dural sinus thrombosis
causing persistent headache in a child, J. Emerg. Trauma Shock 3 (2010) 73–75.
[14] T. Fujita, H. Takeuchi, Y. Iwamoto, Spontaneous disappearance of asymptomatic ce-
rebral venous sinus thrombosis associated with head injury in a child: a case report,
Neurotraumatology 33 (2010) (Jpn, with Eng abstract).
[15] S. Pikis, S. Moscovici, E. Itshayek, J.E. Cohen, Cerebral sinodural thrombosis following
minor head injury in children, J. Clin. Neurosci. 20 (2013) 481–484.
[16] G. Georgoulis, G. Alexiou, N. Prodromou, Sigmoid sinus thrombosis as a sequela of
head injury in children and its management, World Neurosurg. 81 (2014), e7. .
[17] D.C. Lebowitz, M.W. Ko, E.K. Cameron, P.Y. Ko, Cerebral sinus thrombosis in a 6-
year-old boy after a minor head injury, Pediatr. Emerg. Care 30 (2014) 177–179.
[18] A.W. Awad, R. Bhardwaj, Acute posttraumatic pediatric cerebral venous thrombosis:
case report and review of literature, Surg. Neurol. Int. 5 (2014) 53.
[19] G. Rajz, I.B. Zvi, J.E. Cohen, S. Michowiz, Acute epidural hematoma compressing the
dominant sigmoid sinus as an unusual cause of intracranial hypertension: case re-
port and review of literature, OJMN 4 (2014) 76–80.
[20] J.H. Yun, J.H. Ko, M.J. Lee, Early spontaneous recanalization of sigmoid sinus throm-
bosis following a closed head injury in a pediatric patient: a case report and review
of literature, J. Korean Neurosurg. Soc. 58 (2015) 150–154.
[21] M.D. Moharir, M. Shroff, D. Stephens, A.M. Pontigon, A. Chan, D. MacGregor, D.
Mikulis, M. Adams, G. de Veber, Anticoagulants in pediatric cerebral sinovenous
thrombosis: a safety and outcome study, Ann. Neurol. 67 (2010) 590–599.
[22] G. Saposnik, F. Barinagarrementeria, R.D. Brown Jr., C.D. Bushnell, B. Cucchiara, M.
Cushman, G. de Veber, J.M. Ferro, F.Y. Tsai, American Heart Association Stroke Coun-
cil and the Council on Epidemiology and Prevention: diagnosis and management of
cerebral venous sinus thrombosis: a statement for healthcare professionals from the
America Heart Association/American Stroke Association, Stroke 42 (2011)
1158–1192.
[23] C. Apra, O. Kotbi, G. Turc, R. Corns, M. Pagès, R. Souillard-Scémama, E. Dezamis, E.
Parraga, J.F. Meder, X. Sauvageon, B. Devaux, C. Oppenheim, J. Pallud, Presentation
and management of lateral sinus thrombosis following posterior fossa surgery, J.
Neurosurg. (2016) 1–9, http://dx.doi.org/10.3171/2015.11.JNS151881 (Epub ahead
of print).
[24] A. Dalgiç, M. Seçer, F. Ergüngör, O. Okay, R. Akdağ, D. Ciliz, Dural sinus thrombosis
following head injury: report of two cases and review of the literature, Turk
Neurosurg. 18 (2008) 70–77.
[25] A. Tamimi, M. Abu-Elrub, A. Shudifat, Q. Saleh, K. Kharazi, I. Tamimi, Superior sagittal
sinus thrombosis associated with raised intracranial pressure in closed head injury
with depressed skull fracture, Pediatr. Neurosurg. 41 (2005) 237–240.
[26] X. Zhao, A. Rizzo, B. Malek, S. Fakhry, J. Watson, Basilar skull fracture: a risk factor for
transverse/sigmoid venous sinus obstruction, J. Neurotrauma 25 (2008) 104–111.
[27] J. Stam, Thrombosis of the cerebral veins and sinuses, N. Engl. J. Med. 352 (2005)
1791–1798.
[28] H. Yokota, T. Eguchi, M. Nobayashi, T. Nishioka, F. Nishimura, Y. Nikaido, Persistent
intracranial hypertension caused by superior sagittal sinus stenosis following de-
pressed skull fracture. Case report and review of the literature, J. Neurosurg. 104
(2006) 849–852.
[29] Y. Suto, J. Maruya, J. Watanabe, K. Nishimaki, Progressive intracranial hypertension
due to superior sagittal sinus thrombosis following mild head trauma: a case report,
No Shinkei Geka 43 (2015) 629–633 (Jpn, with Eng abstract).
[30] M.H. Meissner, B.K. Zierler, R.O. Bergelin, W.L. Chandler, D.E. Strandness Jr., Coagula-
tion, fibrinolysis, and recanalization after acute deep venous thrombosis, J. Vasc.
Surg. 35 (2002) 278–285.