ORIGINAL CONTRIBUTION

Monitoring of Venous Hemodynamics
in Patients With Cerebral Venous Thrombosis
by Transcranial Doppler Ultrasound
José Manuel Valdueza, MD; Olaf Hoffmann; Markus Weih, MD; Susan Mehraein, MD; Karl Max Einhäupl, MD

Objectives: To test the assumption that transcranial

Doppler ultrasound (TCD) is able to detect and to monitor intracranial venous blood flow velocities in patients
with confirmed cerebral venous thrombosis (CVT).
Design: Prospective case study in 18 patients.
Setting: Inpatient neurologic service in a university

hospital.
Subjects and Methods: Serial TCD examinations were
performed in 18 consecutive patients with CVT (14 females, 4 males) aged 16 to 64 years (mean ± SD,
36.8 ± 13.1 years) during a mean follow-up ranging from
34 to 783 days (mean ± SD, 201 ± 185 days) between 1993
and 1997. Venous TCD was performed with a 2-MHz
range-gated transducer.
Results: Venous blood flow velocities were successfully

measured in all patients. The highest measured velocities
in the monitored intracranial venous vessels ranged from
20 to 150 cm/s (mean ± SD, 58.9 ± 38.8 cm/s), and the lowest were from 9 to 84 cm/s (mean ± SD, 27.9 ± 17.0 cm/s).

D
From the Department of
Neurology, University Hospital
Charité, Humboldt University,
Berlin, Germany.

Fifteen patients (83%) showed a decrease of velocities—2
of them after a transient increase during cessation of heparin therapy. The percentage of velocity decrease ranged
from 34% to 73% (mean ± SD, 56.4% ± 10.9%). A plateau
phase, defined as no further decrease in velocities, was
reached in these patients within 4 to 314 days (mean ± SD,
59.9 ± 73.7 days). Three patients (17%) showed no changes
in velocities as defined by a limit of velocity variation of
30% during the course of CVT. High venous velocities were
significantly associated with altered consciousness
(P = .001). A nonsignificant relationship was observed with
affliction of the superior sagittal sinus. No correlations were
noted for onset of disease, initial motor deficits, and presence of bleeding. No predictive value was gained from analyzing the outcome in relation to absolute velocities or their
decrease.
Conclusions: Serial TCD studies allow monitoring of venous hemodynamics and collateral pathways in patients with CVT. Normal venous velocities in serial measurements, however, do not exclude a diagnosis of CVT.

Arch Neurol. 1999;56:229-234

ESPITE THE evident impor-

tance of venous collateral pathways in cerebral
venous thrombosis
(CVT), the interest in the
assessment of the collateral pathways was
limited. One major reason for this neglect
has been the invasiveness of digital subtraction angiography (DSA) impeding serial examinations. Magnetic resonance
(MR) imaging and MR angiography have
focused new interest in the evaluation and
monitoring of the thrombotic process.1-3
Their usefulness for analyzing hemodynamic properties, however, has been limited until now. Doppler ultrasound techniques have become the standard modality
in the diagnosis and follow-up of thrombotic lesions of other body regions, especially in deep venous thrombosis of the
legs.4 Their application to the cerebral cir-

culation was hindered mainly by bony limitations. In the past few years, however, attempts have been made to assess the normal
cerebral venous circulation by means of
conventional transcranial Doppler ultrasound (TCD),5-8 and transcranial colorcoded duplex sonography.9-12 Furthermore, elevated venous blood flow velocities
have been reported in single adult cases with
thrombotic occlusion of the major venous
outlets.9,13,14 In some instances, follow-up
examinations were performed that demonstrated dynamic changes in venous vessels.15-17 The ability to monitor venous hemodynamics over longer periods has not
yet been shown in a larger group of patients. We intended to prove in a prospective study the assumption that TCD allows the detection and monitoring of blood
flow velocities in venous vessels of patients with confirmed CVT. In addition, we

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PATIENTS AND METHODS
Eighteen consecutive patients (14 females, 4 males)
aged 16 to 64 years (mean ± SD age, 36.8 ± 13.1 years)
with CVT confirmed by DSA and/or MR angiography were examined between 1993 and 1997. Doppler ultrasound was performed with a 2-MHz rangegated transducer (Multidop-X and Multidop-X4;
DWL, Sipplingen, Germany). Almost all studies were
performed by the same examiner (J.M.V.). The examination was performed in the supine position when
using the transtemporal and transorbital approaches. The suboccipital access was performed with
the patient in the supine position with mild elevation of 1 shoulder and the head slightly rotated. Most
of the venous vessels were identified by concomitant insonation of specific arteries. The basal vein of
Rosenthal (BVR) was insonated through the posterior temporal window at a depth of about 60 mm together with the P2 segment of the posterior cerebral
artery. The deep middle cerebral vein (DMCV) was
defined by its proximity to the middle cerebral artery. In both vessels, flow is directed away from the
probe.6 Venous vessels in the anterior parasellar region were insonated through the anterior temporal
window at a depth of 50 to 60 mm or by using the
transorbital route at a depth of 70 mm with a flow
away from the probe. They were defined by their proximity to the internal carotid artery siphon and considered to correspond to the main inflow vessels to
the cavernous sinus (CS), especially to the sphenoparietal sinus or to a sylvian vein.7 The inferior petrosal sinus (IPS) was detected by using the suboccipital approach by its proximity to the basilar artery
at a depth of about 80 to 90 mm with a flow directed
toward the probe.8 The Vmean (the time-averaged mean
velocity over the cardiac cycle of the spectral outline) was automatically recorded in centimeters per
second. Reference values were derived from our own
series,6-8 with a Vmean (±SD) of 11.1 ± 2.7 cm/s in the
DMCV, 10.1 ± 2.3 cm/s in the BVR, 27.3 ± 17.4 cm/s
in the anterior CS inflow region, and 20.8 ± 9.2 cm/s
in the IPS. A definite increase or decrease of velocity
was defined by a change of at least 30%. The pulsatility index was defined as systolic velocity minus diastolic velocity divided by Vmean. For statistical evaluation, paired t tests were performed. A P value less
than .05 was considered significant.

studied the relationship between venous blood flow velocities and severity of disease, site of thrombosis, presence of bleeding, and outcome.
RESULTS

Patient data, neuroimaging results, and TCD findings are
summarized in the Table.
CLINICAL AND NEUROIMAGING FINDINGS
Eighteen patients with proven CVT were examined. A
sudden onset of symptoms was found in 6 patients. Ten

patients presented with a subacute course (up to 4 weeks)
and the remaining 2 patients had a chronic course. Digital subtraction angiography and/or MR angiography revealed thrombosis of the superior sagittal sinus (SSS) in
14 patients, of the lateral sinuses in 17, of the galenic system in 7, and of cortical veins in 2. Nonhemorrhagic venous infarcts were found in 6 patients, and 5 patients had
computed tomographic evidence of hyperdense lesions.
Therapy with heparin with doubling of the partial thromboplastin time, followed by warfarin sodium therapy for
at least 6 months, was the standard treatment.
TCD FINDINGS
All patients underwent 3 to 25 serial TCD examinations
(mean ± SD, 10.4 ± 6.8 times) during a follow-up ranging from 34 to 783 days (mean ± SD, 201 ± 185 days).
Venous signals were detected in all patients. We
intended to insonate a maximum of venous vessels in
each patient. One dominant and frequently insonated
venous vessel was selected for follow-up monitoring.
The inflow pathways to the CS were selected in 11
patients: in 4 of them using the transorbital approach,
the IPS in 3, the BVR in 2, and the DMCV and a vessel
considered to represent the superior petrosal sinus each
in 1 patient. There was a marked increase in Vmean in all
vessels of the patients with CVT compared with the
normal reference values: in the inflow area of the CS,
68.7 ± 41.7 cm/s (n = 11) vs 27.3 ± 17.4 cm/s (P = .007);
in the BVR, 23.0 ± 3.0 cm/s (n = 2) vs 10.1 ± 2.3 cm/s
(P = .07); in the DMCV, 34.0 cm/s (n = 1) vs 11.1 ± 2.7
cm/s; and in the IPS, 40.7 ± 16.4 cm/s (n = 3) vs
20.8 ± 9.2 cm/s (P = .1). A definite decline of Vmean was
obvious during follow-up in all selected vessels. The
measured steady state values, defined as no further
decrease of velocities, were found to be 33.1 ± 21.2 cm/s
in the inflow of the CS (P = .007), 9.5 ± 0.5 cm/s in the
BVR (P = .06), 10.0 cm/s in the DMCV, and 23.3 ± 4.7
cm/s in the IPS (P = .09). There was no difference
between the plateau velocities in patients and the
results of the normal population. Taking all examined
vessels into account, the highest measured velocities
throughout the follow-up ranged from 20 to 150 cm/s
(mean ± SD, 58.9 ± 38.8 cm/s), and the lowest were
from 9 to 84 cm/s (mean ± SD, 27.9 ± 17 cm/s).
Fifteen patients (83%) had a decrease of velocities.
In 2 of them, a transient increase of velocities occurred
during intermittent cessation of high-dose heparin therapy
due to extracranial hemorrhagic complications. The decrease of velocities over time showed a wide variability.
The steady state phase was reached within 4 to 314 days
(mean ± SD, 59.9 ± 73.7 days). Seven patients reached the
plateau phase within 1 month (2 of them during the first
week), 6 further patients within 3 months, 1 patient within
6 months, and 1 within 1 year. The fall of velocities ranged
from 34% to 73% (mean ± SD, 56.4% ± 10.9%). No relevant changes, defined as a limit of velocity variation of
30% during the course of disease, were noted in 3 patients (17%). A clear envelope for recording the pulsatility index could be obtained in about 50% of recordings. The pulsatility index was low, usually ranging
between 0.2 and 0.6. During episodes of elevated intra-

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Summary of Patient, Clinical, and Doppler Data*
Patient No./
Sex/Age, y
1/F/31
2/F/36
3/F/16
4/M/32
5/F/22
6/F/64
7/F/23
8/M/52
9/M/28
10/F/27
11/F/43
12/F/60
13/F/27
14/F/45
15/F/33
16/F/53
17/F/34
18/M/36
Mean ± SD
36.8 ± 13.1 (age)
Range
16-64 (age)

Outcome

Site of
Thrombosis

Follow-up, d

Maximum
Vmean, cm/s

Minimum
Vmean, cm/s

Mean Fall
of Vmean, %

Steady State
Phase, d

Total recovery
Total recovery
Total recovery
Total recovery
Total recovery
Major sequelae
Total recovery
Minor sequelae
Minor sequelae
Total recovery
Minor sequelae
Total recovery
Total recovery
Major sequelae
Minor sequelae
Total recovery
Total recovery
Total recovery

SSS, R-TS, SS, DV
L-TS, CV
SSS, R-TS
R-TS
TS, SS, DV
SSS, R-TS, L-TS, CV
SSS, R-TS, SS
SSS, R-TS
SSS, SS, DV
SSS
L-TS, SS, DV
SSS, R-TS, L-TS
SSS, L-TS, SS
SSS, R-TS, L-TS, SS
SSS, R-TS, L-TS
SSS, R-TS
SSS, R-TS
SSS, R-TS

97
60
305
286
190
87
31
8
34
453
265
185
43
37
783
70
142
155

150
20
20
24
25
50
75
24
35
63
103
58
35
120
26
95
34
104

60
12
9
20
15
24
20
20
23
30
40
24
20
48
10
84
10
34

60
40
55
17
40
52
73
17
34
52
61
58
62
60
61
10
71
67

4
30
76
†
110
21
16
†
34
314
53
50
43
7
26
†
86
29

...

...

201 ± 185

58.9 ± 38.8

27.9 ± 17.0

56.4 ± 10.9‡

59.9 ± 73.7

...

...

34-783

20-150

9-84

34-73

4-314

*Vmean indicates time-averaged mean velocity over the cardiac cycle of the spectral outline; R, right; L, left; SSS, superior sagittal sinus; SS, straight sinus;
TS, transverse sinus; DV, deep veins; CV, cortical veins; and ellipses, not applicable.
†Not considered because the variation of velocity was ,30%.
‡The values of patients 4, 8, and 16 are not included.

cranial pressure, the arterial Doppler spectra revealed a
higher pulsatility transiently. The arterial blood flow velocities usually remained in the normal range.
In cases of SSS thrombosis, higher velocities were
found than in cases of thrombosis at other locations (63.5
vs 43.0 cm/s). Velocities were also higher in complete
occlusions as compared with partial occlusions (71.6 vs
59.0 cm/s). However, these differences did not reach statistical significance. Initial impairment of consciousness, on the other hand, was significantly associated
(P = .001) with higher venous velocities (119.3 vs 41.1
cm/s). No obvious relationship was seen between venous velocities and the presence of motor deficits or bleeding. Outcome was not correlated to the initial range of
velocities or to the degree of regression.
ILLUSTRATIVE CASE
A 31-year-old woman (patient 1) presented with a 5day history of elevated intracranial pressure. On admission, she complained of headaches and double vision.
Clinically, she was alert and had a left-sided hemiparesis. A native computed tomographic scan was unremarkable. Digital subtraction angiography revealed CVT with
major affliction of the SSS, the straight sinus, the right
transverse sinus, and the deep internal veins (Figure 1,
top). On transtemporal TCD examination, a prominent
venous signal with a velocity of 150 cm/s and a flow directed away from the probe, considered to represent an
inflow vessel to the CS, was found in the left parasellar
region at a depth of 52 to 62 mm. Partial thromboplastin time–adjusted high-dose heparin therapy was followed by clinical normalization within 48 hours. Dur-

ing the first 4 days, the venous Vmean dropped to values
between 60 and 70 cm/s and remained in this range during the following week (Figure 2).Two weeks after admission, she developed clinical signs of tentorial herniation. A right-sided subdural hematoma was seen on
computed tomography with midline shift and marked
brain edema. Venous blood flow velocities remained unchanged during that time, suggesting a nonthrombotic
cause of the subdural hematoma, which was confirmed
on repeated angiography (Figure 1, bottom). During cessation of heparin treatment after surgery, the velocities
increased transiently to 105 cm/s, reaching again steady
state values of 60 to 70 cm/s during adjusted anticoagulation (Figure 3). The patient’s condition normalized
within 6 weeks and she was discharged from the hospital with warfarin medication. During a follow-up of 97
days, the venous velocities remained substantially unchanged.
COMMENT

Many aspects regarding the pathophysiology of CVT are
not well understood.18,19 Considering similar mechanisms as in deep vein thrombosis, however, an evolving
process with instantaneous changes of venous hemodynamics has to be assumed due to continuous recanalization and subsequent new thrombus formation. The severity of the disease seems—apart from the site of the
occlusion—to depend on the time course of the thrombus formation and the capacity to build up a compensatory venous circulation. This may be by using preexisting nonaffected veins and sinuses and/or by opening up
of collaterals. In contrast to the dural sinuses, the cere-

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160
140

Vmean, cm/s

120
100
80
60
40
20
0
0

20

40

60

80

100

Time, d

Figure 3. Time course of mean venous blood flow velocities (Vmean) in
patient 1.

measurements of the venous system will probably further contribute to the assessment of the dynamic aspects of CVT.20,21
NORMAL VENOUS BLOOD FLOW VELOCITIES

Figure 1. Angiogram of lateral venous phase of left carotid artery
demonstrating severe cerebral venous thrombosis in patient 1 with extensive
filling defect of the superior sagittal sinus and the galenic system (top). A
marked improvement is seen on repeated angiography after 2 weeks of
anticoagulation therapy with a prominent venous drainage into the
sphenoparietal sinus (small arrow), cavernous sinus (large arrow), and
inferior petrosal sinus (curved arrow) (bottom).

50

Vmean = 150 cm/s
Depth = 60 mm

0

Venous Blood
Flow Velocity, cm/s

50
100
150

50

Vmean = 70 cm/s

0
50
100

Figure 2. Venous transcranial Doppler ultrasound revealing mean venous
blood flow velocities (Vmean) of 150 cm/s in patient 1 (top) that decreased to a
plateau of about 70 cm/s within 4 days of anticoagulation therapy (bottom).
A transient elevation occurred after evacuation of subdural hematoma and
cessation of anticoagulant therapy. Arrows indicate flow away from the
probe.

bral veins are able to extend their walls. Thus, dilation
of the veins may be seen as an indirect sign of CVT on
DSA examination. The dynamic aspects of CVT, however, cannot be studied in follow-up examinations by DSA
due to its invasiveness. Magnetic resonance imaging and
MR angiography offer an important advance as diagnostic and follow-up instruments. Visualization of vessels,
however, does not necessarily correspond to the vessels’
functional status. The additional application of MR flow

In the past years, normal venous Vmean values were established in various cerebral veins and sinuses in adults
by Doppler ultrasound methods. The recognition of the
venous character of an intracranial Doppler signal can
be assured by its typical low pulsatile flow with a pulsatility index ranging between 0.2 and 0.5, its reaction pattern during the Valsalva test demonstrating marked transients of flow velocities, and the whispering sound clearly
different from an arterial signal. Using TCD, venous vessels are identified by their known anatomical relationship to certain arteries, eg, the DMCV to the middle cerebral artery, the BVR to the posterior cerebral artery, the
inflow vessels to the CS to the carotid siphon, and the
IPS to the basilar artery. Normal venous Vmean values have
been reported to be 11.1 ± 2.7 cm/s in the DMCV,
10.1 ± 2.3 cm/s in the BVR,6 27.3 ± 17.4 cm/s in the anterior CS inflow7 through a transtemporal approach, and
20.8 ± 9.2 cm/s in the IPS via a suboccipital approach.8
Similar values in the DMCV and the BVR have been reported using transcranial color-coded duplex sonography.12 The straight sinus was not studied in our series
because of its limited transoccipital accessibility. On
transoccipital insonation of the straight sinus, a Vmean of
the straight sinus of 20.0 ± 3.0 cm/s using TCD5 and a peak
velocity of 35.0 cm/s using transcranial color-coded duplex sonography11 were obtained. By using a transtemporal approach, the straight sinus revealed a lower peak
velocity of 19.1 ± 6.1 cm/s.9,12
VENOUS VELOCITIES IN CVT
In SSS thrombosis, a Vmean in the BVR ranging from 19.5
to 43.0 cm/s was reported in 3 and 4 patients, respectively, by single TCD measurements.13,17 Using colorcoded transcranial color-coded duplex sonography via
a temporal access, venous peak velocities of 83.0 and 92.0
cm/s were found in the straight sinus.9 Significant differences of venous blood flow velocities in patients with
thrombosis of the transverse sinus were reported using
echocontrast-enhanced transcranial color-coded du-

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plex sonography. Peak velocities were found to be
28.4 ± 6.5 cm/s in the nonaffected transverse sinus and
9.4 ± 4.0 cm/s in the hypoplastic or partially occluded
transverse sinus.14
The interpretation of venous hemodynamics from
single observations, however, may be limited by the high
variability of normal venous blood flow velocities, which
is of special relevance in the inflow area of the CS. In our
series of long-term follow-up examinations, a marked decrease of velocities during the course of the disease was
noted in 15 patients (83%). Elevated venous velocities
were thought to correspond to the venous collateral pathways that were also documented on angiography. Especially in patients with marked venous signals at the CS
and affliction of the SSS, DSA depicted a prominent sphenoparietal sinus, CS, and IPS in the majority of cases. A
steady state was achieved after 4 to 314 days (mean, 59.9
days), which indicates that the hemodynamic changes
may last several months, but may also be resolved within
a few days. A variety of morphologic changes over time
has also been found in MR studies: the thrombus may
be resolved or partially reopened within several weeks.22,23
Complete recanalization has been observed in 2 series
after 6 months in 3 of 10 patients1 and 5 of 8 patients.2
Abnormalities, however, may be present for years.3 Considering the MR data, a steady state of venous blood flow
velocities seems to represent the point in time when adequate collateralization is achieved rather than indicating complete resolution of the thrombus.
Two of our patients experienced a rise of velocities
during perioperative interruption of intravenous heparin therapy. In at least 1 of them, the interruption was
followed by a severe progress of CVT, which adds further evidence of the importance of anticoagulation.19,24
No changes were noted in 3 patients, with 1 of them
exhibiting symptoms of pseudotumor cerebri starting 3
months before admission, and the other 2 experiencing
mild symptoms and clinical signs. Thus, normal blood
flow velocities in examined venous vessels do not
exclude CVT. This was also shown in 2 of 6 patients
with SSS thrombosis by analyzing the BVR and
DMCV.13 It seems, however, that velocities in the normal range are associated with a less severe clinical presentation and more chronic evolution. On the other
hand, high venous velocities—especially measured at
the CS inflow—are not necessarily a sign of compromised venous hemodynamics.
In 11 patients, the area of the CS was chosen as the
reference vessel for follow-up. Using DSA and MR angiography, this area was identified as the most relevant
drainage pathway in CVT independent of the site of
thrombosis. The IPS was selected in 3 patients. It usually communicates with the sphenoparietal sinus via the
CS and has the advantage of only moderate variations of
normal velocities. However, because of the necessity to
manipulate the head position during the examination,
this approach cannot be recommended in severely affected patients. The BVR was selected for monitoring purposes in 2 patients. This vessel is not difficult to insonate. From angiographic studies in cases of SSS
thrombosis, it is evident that the basal veins form a part
of the compensatory circulation. However, due to the abil-

ity of the vein to dilate, the rise in venous blood flow velocity may be limited. Consequently, normal velocities
in the BVR do not exclude elevated flow in this vessel.
In our series, only 7 of 14 patients with a clearly demonstrable BVR and otherwise elevated venous velocities had
elevated velocities in the BVR. In 1 patient with occlusion of the straight sinus, the BVR revealed a reverse flow.
This type of collateralization is shown on DSA in patients with occlusion of the straight sinus due to meningiomas25 and in deep-seated arteriovenous malformations26 and has also been observed in 1 infant with
thrombosis of the straight sinus.27 One prominent signal was found using a posterior temporal approach that
could not be assigned to a specific vessel. From the selected Doppler settings and angiographic findings, insonation of the superior petrosal sinus was assumed.
LIMITATIONS
Increasing bony thickness in elderly patients may hinder
the insonation of intracranial vessels. As CVT is usually
encountered in patients of younger age, this will be a minor limitation. In our series, only in 1 patient was there
no detectable signal transtemporally. Follow-up studies
should require a reliable anatomical identification of the
insonated vessels. This was not achieved in many patients when monitoring the inflow region of the CS. Vessel identification problems may be overcome by transcranial color-coded duplex sonography. However, a
significantly lower detection rate using transcranial colorcoded duplex sonography has to be considered.28 By using echo-contrast agents, the detection rate of intracranial venous vessels will improve. Furthermore, raised
intracranial pressure may alter venous hemodynamics and
flow velocities. Localized brain edema may also cause vessel displacement, leading to uncertainties in vessel identification. For follow-up examinations, however, it seems
more important to define a reference venous vessel using constant Doppler settings, ie, probe position, depth,
sample volume, and relationship to arterial signals, than
to be sure of its designation. Finally, the large variation
in normal venous velocities, especially in the inflow area
of the CS, is also a major obstacle hindering a simple interpretation of velocity data.
CONCLUSIONS

The present study provides further support that TCD enables serial venous velocity measurements in venous collateral pathways in patients with CVT. There was an obvious relationship between initially high venous flow
velocities and severity of disease, but not with outcome.
Early regression of velocities was not found to indicate
a favorable prognosis, but could be observed in the majority of cases. Transcranial Doppler ultrasound cannot
replace the diagnostic value of angiography or MR modalities; however, it may offer the possibility to evaluate
noninvasively dynamic changes in the venous circulation of the brain in normal and altered states. Whether
the assessment of functional parameters of venous hemodynamics in CVT will influence decisions on therapy
and its duration has to be investigated in future studies.

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Accepted for publication May 21, 1998.
Reprints: José Manuel Valdueza, MD, Department of
Neurology, University Hospital Charité, Humboldt University, Schumannstrasse 20/21, 10117 Berlin, Germany
(e-mail: Valdueza@neuro.charite.hu-berlin.de).
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