CASE REPORT
headache, dural sinus, thrombosis

Cerebral Dural Sinus Thrombosis
Cerebral dural sinus thrombosis is an unusual syndrome in which a patient presents with a severe headache that may be associated with diverse
neurologic and physical findings. The case of a 31-year-old woman with
headache, vomiting, generalized tonic-clonic seizure, and s u b s e q u e n t
dense hemiplegia is presented. The patient was diagnosed as having a cerebral dural sinus thrombosis, but only after the diagnosis was missed
initdally. The syndrome m a y be difficult to detect because it can mimic
several other entities. There are several known or suspected predisposing
factors. The syndrome, diagnostic modalities, and therapeutic options are
reviewed. [Pannke TS: Cerebral dural sinus thrombosis. Ann Emerg Med
July I991;20:813-816.]

Thomas S Pannke, MD
Peoria, Illinois

INTRODUCTION
Severe headache represents a fairly c o m m o n complaint among emer gency department patients. Patients with the history of "migraines" are
seen frequently. Careful history will usually allow differentiation between
the patient's usual headache and more serious headaches. Cerebral dural
sinus thrombosis (CDST) is an uncommon syndrome that can cause severe
headache. The presentation of the disease can vary from headache alone to
generalized seizures followed by focal deficits. There are several known or
suspected predisposing factors. The case of a 31-year-old woman with a
history of migraine whose course with CDST was fairly typical is presented, illustrating some of the possible clinical presentations as well as a
successful treatment plan.

Address for reprints: Thomas S Pannke,
MD, University of Illinois College of
Medicine at Peoria, Emergency Medicine
Residency Program, St Francis Medical
Center, 530 Northeast Glen Oak, Peoria,
Illinois 61637.

From the Emergency Medicine Residency
Program, University of Illinois College of
Medicine at Peoria.
Received for publication August 21, 1990.
Revision received February 5, 1991.
Accepted for publication February 18,
1991.

CASE REPORT
A 31-year-old woman presented to another ED complaining of intermittent headache for one week and vomiting for two days. On the day of admission, she was awakened from sleep by a severe headache. She was
transferred to our hospital with the diagnosis of possible subarachnoid
hemorrhage. The patient had a significant history of recurrent "migraine"type headaches for which previous workup had been negative. These migrainous headaches had resulted in several ED visits over the previous year
for parenteral narcotic analgesia. Medications included oral contraceptive
pills, prazepam, and piroxicam. The patient denied any other neurologic
symptoms.
Examination revealed a supple neck, normal fundi, and normal neurologic examination. Computed tomography (CT) did not reveal an intracranial bleed or other pathology. A lumbar puncture revealed an opening
pressure of 44 cm cerebrospinal fluid, 726 RBCs, and two WBCs. Protein
was 55 mg/dL (550 rag/L), and glucose was 56 mg/dL (3.0 mmol/L).
The patient was hospitalized, and workup included magnetic resonance
imaging (MRI} of head and neck and cerebral angiography that revealed no
pathology. Her headache improved over the course of a week. She was discharged with an improved headache and instructed to take acetazolamide
and return for follow-up in one week. The discharge diagnosis was probable migraine headache, although a dural sinus thrombosis had been suspected.
One day after discharge, the patient presented by advanced life support
personnel to the ED complaining of a five-minute generalized tonic-clonic

20:7 July 1991

Annals of Emergency Medicine

813/161

THROMBOSIS
Pannke

FIGURE 1. Diagram of cerebral du-

ral sinuses. (Hollinshead WH, Rosse
C: Textbook of Anatomy, ed 4. Philadelphia, JB Lippincott Co, 1985, p
925. Used with permission.)

~ittol

Interca~

=lmic v.
Sphenopari,

seizure and subsequent dense right
hemiplegia and slurred speech. She
denied any trauma, febrile illness, or
family history for seizures.
On examination, she was dysarthric, dense right hemiplegia with
right ankle clonus was found, and
t h e r e was no p a p i l l e d e m a . U n enhanced CT scan in the ED was interpreted by a radiologist as normal.
She was admitted, and IV loading
with phenytoin was carried out.
The follow-up MRI revealed extensive t h r o m b o s i s in the sagittal,
straight, and jugular sinuses. These
findings were confirmed by cerebral
angiography. The patient was placed
on heparin and mannitol and continued on phenytoin with subsequent
resolution of her hemiplegia during
the next two days. No further seizures were noted. On the third hospital day, she was c h a n g e d f r o m
heparin to warfarin. The patient subs e q u e n t l y was f o u n d to have an
a s y m p t o m a t i c left f r o n t a l i n t r a cranial hemorrhage on a routine follow-up MRI. She made a complete
recovery and was instructed to avoid
any future use of oral contraceptives.
She was discharged home on phenytoin, warfarin, and acetaminophen/
hydrocodone for headache.
DISCUSSION
The diagnosis of CDST must be
considered in patients complaining
of unusual headaches, new-onset seizures, and focal neurologic deficits.
Patients may present with headache
alone or have v o m i t i n g , seizure,
hemiparesis or hemiplegia, blurred
vision, or other neurologic symptoms. These headaches are not location specific; however, they are typically severe. The seizures may be
focal or generalized. Physical examination may reveal the above neurologic deficits; diplopia from a falsely
localizing sixth nerve palsy, a homonymous hemianopsia, papilledema,
occasional fever, and nuchal rigidity.
Lumbar p u n c t u r e m a y reveal increased opening pressure, increased
protein, or increased RBCs.I
The anatomy of the cerebral sinuses is shown (Figure 1). Our patient
had a superior sagittal sinus throm162/814

,ernou$

Basilar plexu
*.iddle
leningeol
Inferior
petrosal
Superior
petrosal
Petrosquomous

Sigmoid

Tr

Superior sagittal

bosis that extended into the straight
and jugular sinuses.
A thrombus in the cavernous sinus, most often seen after infection
of the ethmoid, maxillary, or sphenoid sinuses or of the facial skin, can
present with headaches; cranial
nerve findings of III, IV, V-ophthalamic, and VI involvement; and papilledema. Also seen with cavernous
sinus thrombosis are high fluctuating
fevers, edema of the forehead and
eyelids, and chemosis and proptosis.
Hemiplegia, dysarthria, or seizure re~
sulting from an uncomplicated cavernous sinus thrombosis are unlikely
to be seen.
A review of 38 cases revealed that
there are two important groups of patients with CDST. The first group
typically has headache and papilledema. The second group has, in addition, vomiting, seizures, and focal
neurologic deficits. The two groups
are thought to represent thrombus in
the sinus alone in the former and extension of thrombus into the cortical
veins in the latter. 1 These two groups
may be important prognostically but
clinically represent different phases
of the syndrome. Other s y m p t o m s
that might be seen include numbness, paresthesias, visual disturbances, aphasia or dysarthria, lethAnnals of Emergency Medicine

" Confluence of sinuses

argy, and coma. Those presenting
with seizure and focal deficits may
do worse than those with headache
alone. 1
This p a t i e n t p r e s u m a b l y had a
headache from CDST during her first
admission that escaped detection, despite appropriate diagnostic workup.
After she had a seizure and neurologic deficit, the diagnosis was made
using the same workup. This case
demonstrates the natural history of a
typical presentation for CDST.
There have been m a n y proposed,
predisposing factors for this disease,
most of which involve a state of hypercoagulability. These include cancer a and possibly chemotherapy, a the
postpartum state,< s oral contraceptive use, l, 6-9 regional enteritis, lo and
infection with dehydration. 11 Our patient had a history of "migraines"
and was taking an oral contraceptive.
It has long been thought that migraine headache is a relative contraindication to use of oral contraceptives; however, this has not been
studied conclusively. 12 As many as
20% of reported cases of CDST have
no etiology found after workup.
Diagnostic modalities have
changed with the advent of MRI. CT
with enhancement can detect 80% of
CDST. 1 The most important finding
20:7 July 1991

hh
Pannke

FIGURE 2. A. Contrast-enhanced C T

TABLE. Headache type
Signs

CDST

Cavernous Sinus
Thrombosis

Fever

+

+ + +

0

+

Papilledema

+ + +

+ + +

0

+ +

Infection*

+

+ + +

0

0

+ +

Migraine

Subarachnoid
Hemorrhage

Symptoms
Vomiting

+ + +

O

+ +

Seizure

+ +

0

0

+ +

Hemiplegia

+ +

0

+

+ +

Dysarthria

+ +

0

+

+ +

Cranial newest

+

+ + +

0

+

Coma or altered mental status

+ +

0

0

+ + +

+ + +, very common; + +, somewhatcommon; +, seen only occasionally; O, unusual.
*Infection elsewherein body
tCranial nerve involvement, often II1, IV, V, VI in cavernous sinus thrombosis, and occasionally falsely localizing VI in CDSI

on an enhanced CT is the "empty
delta sign" seen in 28% to 35% of
patients (Figure 2), 13,14 This sign represents a clot within the sinus and
contrast material in the smaller veins
within the wall of the sinus. Falsepositives may be seen if there is adjacent subdural hematoma, subdural
empyema, subarachnoid hemorrhage,
or dural sinus septation. 14 An un20:7: July 1991

enhanced CT scan, as might be done
in the w o r k u p of a possible subarachnoid bleed, may reveal small
ventricles in about 33% 13 and the
"cord" or "dense vein" sign in 6% to
20%.13,14 The classic recommendation had been to follow any negative
scans in suspicious individuals with
cerebral angiography. 13
CT scanning probably represents
Annals of Emergency Medicine

scan. B. M R [ s c a n d i s p l a y i n g t h e
"'empty delta sign." This sign represents a clot w i t h i n the superior sagittal sinus.

the first line of diagnosis for use in
the ED because it is generally available and can detect CDST as well as
other pathology. MRI provides improved capabilities over the CT scan
for the diagnosis of CDST as well as
other potential causes for a patient's
symptoms. Even though it is a new
modality with only limited information in the literature, MRI appears to
be the best modality available for the
diagnosis of CDST.15,16 Angiographic
follow-up to negative MRI scans is
r e c o m m e n d e d at this time. 17 The
workup for our patient included all
of these diagnostic modalities. Her
initial presentation was considered
to be clinically a result of CDST, but
the diagnosis was not proven. The
reason for this possibly missed diagnosis remains elusive even after retrospective review.
The differential diagnosis for a patient presenting with a severe head815/163

THROMBOSIS
Pannke

ache should include subarachnoid
hemorrhage, herald bleed (thunderclap headache), unsuspected subdural
or epidural hemorrhage, cavernous
sinus thrombosis, vascular cephalgia,
pseudotumor cerebri, stroke, tumor,
and meningitis. The unenhanced CT
with follow-up lumbar puncture can
help with the diagnosis, but a high
index of clinical suspicion is needed
to make the diagnosis in a patient
with a CDST (Table).
Therapy is probably the most controversial aspect of any discussion of
CDST. There have been reports of
successful therapy using urokinase to
lyse the thrombus, either locally or
systemically.18,19 Some advocate anticoagulation alone, 2o whereas others
oppose anticoagulation and propose
steroid or antiseizure medication. 21
The use of mannitol with or without
anticoagulation also has been proposed, 8 as has barbiturate coma with
ventricular drainage. 22 The use of
surgical evacuation appears to be
more of historical interest. This case
was managed successfully with the
use of combination therapy that included antiseizure and anticoagulant
medication and an osmotic diuretic.
The development of an asymptomatic intracranial h e m o r r h a g e was
noted, but this did not affect the
eventual outcome.
The prognosis for a patient with
dural venous sinus t h r o m b o s i s is
fairly good. Recent literature has reported a mortality rate of 10% with
several different therapeutic interventions. Morbidity in the form of
blindness, resulting from optic atrophy, and focal motor deficits occur in
6% to 20% of patients. Factors found
to correlate well with poor outcome
are the initial presence of focal symptoms. 1 Our patient developed focal
deficits but suffered no adverse sequelae.

164/816

From a single case, no conclusion
about the best therapy can be made.
The use of anticoagulation to prevent
clot extension makes empiric sense,
but it must be balanced against the
risk of intracranial bleed in a patient
with increased intracranial pressure
and venous congestion. There is a
theoretic argument against using an
osmotic diuretic because dehydration
is often implicated as a contributing
factor in the development of CDST.
In this case, mannitol was used to
decrease the high intracranial pressure that had been detected by the
lumbar puncture.

SUMMARY
A case of CDST is presented. The
patient had a typical presentation of
the syndrome. Successful diagnosis
using enhanced CT, MRI, and angiography was demonstrated. Management directed at the pathologic
derangements using heparin, warfarin, p h e n y t o i n , and m a n n i t o l
brought about resolution of the patient's s y m p t o m s . No therapeutic
conclusions can be reached from this
case. There are several reports of
CDST in patients who take oral contraceptive medication, and it is believed that this contributed to the patient's development of the syndrome.
This case is presented to illustrate a
possible diagnosis for a patient with
severe headache and, in particular,
new neurologic deficits.

REFERENCES

1982; 73: 740-749.
4. Estanol B, Rodriguez A, Conte G, et ah Intracranial
venous thrombosis in young women. Stroke 1979;
10:680-684.
5. Vali A, McKinstrey C, Dick D: Case of the month: A
fit in a young woman. Br J Radiol 1988~61:335-336.
6. Atkinson E, Fairburn B, Heathfield K: Intracraniai
venous thrombosis as complication of oral contraception. Lancet 1970;1:914-918.
7. Haley E, Brashear H, Barth J, et al: Deep cerebral
venous thrombosis: Clinical, neuroradiological, and
neuropsychological correlates. Arch Neuro] 1989;46:
337-340.
8. Beal M, Wechsler L, Davis K: Cerebral vein thromBosis and multiple intracranial hemorrhages by computed tomography. Arch Neurol 1982;39:437-438.
9. Goldberg A, Rosenbaum A, Wang H, et al: Computed
tomography of dural sinus thrombosis. J Comput Assist
Tomogr 1986;10:16-20.
10. 8igsbee B, Rottenberg D: SagittaI sinus thrombosis
as a complication of regional enteritis. Ann Neuro]
1978;3:450-452.
1L Gum G, Numaguchi Y, Foster R, et al: Superior sagittal sinus thrombosis with intracerebral hematoma.
Comput Radiol 1987;11:199-202.
12. Benson M, Rebar R: Relationship of migraine head ~
ache and stroke to orai contraceptive use. J Reprod Med
1986; 12:1082-1088.
13. Rao K, Knipp H, Wagner E: Computed tomographic
findings in cerebral sinus and venous thrombosis. Radiology 1981~140:391-398.
14. Virapongse C, Cazenave C, Quisling R, et al: The
empty delta sign: Frequency and significance in 76
cases of dural sinus thrombosis. Radiology 1987;162:
779W85.
15. Macchi P, Grossman R, Gomori J, et al: High field
MR imaging of cerebral venous thrombosis. J CompL2t
Assist Tomogr 1986;10:10-15.
16. McMurdo S, Brant-Zawadzki M, Bradley W, et al:
Dural sinus thrombosis: Study using intermediate field
strength MR imaging. Radiology 1986;161:83-86.
17. Bauer W, EinhaupI K, Heywang S, et al: MR of
venous sinus thrombosis: A case report. A m J Nncl Radiol 1987;8:713-715.
18. Scott J, Pascuzzi R, Hall P, et ah Treatment of dural
sinus thrombosis with local urokinase infusion. J Nezz~
rosLlrg 1988;68:284-287.
19. DiRoceo C, Iannelli A, Leone G, et al: Heparinurokinase treatment in aseptic dural sinus thrombosis.
Arch Neuroi i981;38:431-435.

I. Bousser M, Chiras J, Bories J, et al: Cerebral venous
thrombosis - A review of 38 cases. Stroke 1985;16:
199-213.

20. Castaigne P, Laplane D, Bousser M: Superior sagittal sinus thrombosis (letter). Arch Netlrol 1977;84:
788-789.

2. Sigsbee B, Deck M, Posner J: Nonmetastatic superior
sagittal sinus thrombosis complicating systemic cancer.
Ne~Irology 1979;29:139-146.

21. Gettelfinger D, Kokmen E: Superior sagittaI sinus
thrombosis. Arch Nenrol 1977;34:2-6.

3. Hickey W, Garnick M, Henderson I, et al: Primary
cerebral venous thrombosis in patients with cancer - A
rarely diagnosed paraneoplastic syndrome. A m J Med

Annals of Emergency Medicine

22. Hanley D, Feldman E, Borel C, et al: Treatment of
sagittal sinus thrombosis associated with cerebral hemorrhage and intracrania] hyperteusion. Stroke 1988;
19:903-909.

20:7 July 1991