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Special Venous Anatomy and Ultrasound Anatomy 45
Fig. A2.78 A Schematic drawing, sagittal plane: Note the blue-col-
ored ICV in its distal part. B TCCS, transtemporal approach, thalamic
to cella media axial plane. Color-mode imaging of the contralateral
ICV as a small red-coded segment over the thalamic roof. Note the
ipsilateral thalamus (semicircle line). C CTA, axial MIP. Note the ICV
merging into the VG (arrows). D Doppler spectrum analysis of the
ICV (flow velocity: 13/10 cm/s) with a flow towards the probe.
Vein of Galen (VG)
Anatomic details: TheVGislocatedinthequadrigeminal
cistern. It is a short unpaired vessel draining into the StS.
The angle between the VG and the StS varies between > 90°
(10 % of cases), 30–90° (60 % of cases) and < 30° (30 % of
cases).
Position and vessel identification: The VG can be insonated through the transtemporal bone window using an
axial thalamic insonation plane posterior to the hyperechogenic pineal gland. It can also be found by following
the signal of the BVR until its junction with the VG
(Fig. A2.79). The point, where the VG turns into the StS
can usually not be visualized. Reported success rates for VG
insonation vary from 30 % to 90 %.
Normal values: Flow velocities: See Ta b l e A 2.8 (p. 53).
Fig. A2.79 A Schematic drawing, sagittal plane. Note the blue-col-
ored VG. B TCCS, transtemporal approach, thalamic to cella media
axial plane. Color-mode imaging of the VG as a small blue-coded
segment posterior to the hyperechogenic pineal gland. C CTA, axial
MIP. Noteboth ICVand BVR merging into the VG(arrows). D Doppler
spectrum analysis of the VG (flow velocity: 11/8 cm/s) with a flow
away from the probe.
Fig. A2.80 MR T2-weighted images, axial (A )andcoronal(B )
planes. MR ce T1-weighted image, sagittal plane (C ): Insonation
field and transducer position for examination of the StS, TS, and SSS.
Straight Sinus
Anatomic details: The StS is a mainly unpaired, triangular
vessel with a median length of 50 mm. It arises from the
merging VGs and the ISS and descends toward the confluence of sinuses where it frequently drains into the confluence or into preferably the left TS. A double lumen is
found in approximately 15% of cases. Aplasias are exceptionally rare.
Position and vessel identification: The proximal StS, like
the VG, is insonated through the transtemporal bone window in an axial thalamic plane. However, to visualize a
longitudinal segment the transducer position has to be
adapted by turning it in a line between the pineal gland
and the internal occipital protuberance to achieve an ob-
lique axial insonation plane. Therefore, the dorsal part of
the transducer has to be tilted downward (Fig.A2.80).
Flow velocities should be recorded from the middle segment of the vessel (Fig. A2.81) to avoid confusion with the
VG or the confluence of sinuses. Flow turbulences and
raised velocities may be seen in its proximal part presumably caused by a lumen narrowing within the StS inflow
region because of large pacchionian granulations
(Fig. A2.82). The reported rates of detection vary between
50 % and 80 %.
Normal values Flow velocities: see Table A2.8 (p.53).
2 Vascular Anatomy and Structure of Ultrasound Examination46
Fig. A2.81 A Schematic drawing, sagittal plane. Note the blue-col-
ored StS. B TCCS, transtemporal approach, thalamic to lower pontine oblique axial plane. Color-mode imaging of the distal StS visible
as a blue-coded segment pointing toward the hyperechogenic internal occipital protuberance. C CTA, lateral midsagittal MIP. Note
the StS (arrows). D Doppler spectrum analysis of the StS (flow
velocity: 13/10 cm/s) with a flow away from the probe.
Fig. A2.83 Schematic drawing of the main drainage patterns of the
SSS and StS and anatomical variants of the CoS.
Confluence of Sinuses, Transverse Sinus, and Superior
Sagittal Sinus
Anatomic details: Theconfluenceofsinusesisoneofthe
main venous blood distributors located directly in front of
internal occipital protuberance. It collects blood from the
superficial venous system via the SSS as well as from the
deep venous drainage system via the StS and connects
both with each other. From there it transfers the blood
via the paired TS and SiS into both IJVs. However a “perfect” CoS only exists in about 20 % of cases (Fig.A2.83).
Divergent results have been published in regard to variants and its prevalence. It seems however clear that
Fig. A2.82 Top, left: CTA, lateral midsagittal MIP. Note the lack of
contrast in the transitional region between VG and StS which indicates a large pacchionian granulation (arrow). Top, right: Color
mode imaging of the transition between the BVR, VG, and the StS.
Note the aliasing phenomenon in the proximal StS (arrow). Bottom:
TCCS, transtemporal approach, thalamic plane. Color-mode imaging
Doppler spectrum analysis of the StS revealing a nonpathologic
elevated venous flow velocity (flow velocity: 71/42 cm/s) which is
probably caused by a large pacchionian granulation.
mostly, the drainage is asymmetric with the SSS more
frequently passing the blood into the right TS and the StS
draining into the left TS. A complete separation of superficial and deep venous drainage which means that no CoS
is present can be assumed in about 10 % of cases but has
also been reported in up more than 20 % (Bisaria 1985,
Hempel and Elmohamed 1971). Occasionally the confluenceofsinusesmaybeavenousplexusratherthena
singular vessel junction. The adjacent TS runs horizontally
from the internal occipital protuberance to the edge of the
petrousbonepyramidwhereitturnsdownwardtobecome the SiS. Differences between the right and left sides
are frequent. Aplasias have been reported in conventional
angiography from 0.5 % to 3 % on the right and from 2 % to
14% on the left. Higher values have been published based
on MRA, ranging from 4 % on the right to 20 % on the left
side, which reflects the lower sensitivity of MRA (Alper et
al. 2004; Durgun et al. 1993; Hacker 1974). With regard to
the diameter, a right-sided dominance is found in about
50 % of cases and a left-sided dominance in 25 % of cases.
Bilaterally symmetric transverse sinuses are observed in
the remaining 25 % of cases.
Position and vessel identification: The TS, CoS, and distal
partoftheSSScanbevisualizedthroughthetranstemporal bone window in a modified thalamic, midbrain or
upper pontine axial plane (Fig.A2.80). Best results are
achieved for the TS if the contralateral side is insonated.
At first, the insonation depth has to be increased up to
14cm to visualize the contralateral skull and the hyperechogenic internal occipital protuberance. Then, a small
color window with low or maximal reduced PRF is placed
Special Venous Anatomy and Ultrasound Anatomy 47
Fig. A2.84 A Schematic drawing, axial plane. Note the blue-colored
contralateral and ipsilateral TS as well as the CoS. B TCCS, trans temporal approach, midbrain to lower pontine oblique axial plane.
Color-mode imaging of the blue-coded contralateral TS over a
length of several centimeters. C MR contrast-enhanced T1weighted image, axial MIP. Note one hypoplastic TS (arrows).
D Top: Doppler spectrum analysis of contralateral (left) TS at rest
(flow velocity: 17/12 cm/s) with a flow away from the probe. Bottom
left: Increase of flow during right-sided IJV compression. Bottom
right: Interruption of flow during left-sided IJV compression.
above the presumed CoS. The contralateral TS is identified
with a signal away from the probe close to the skull. In
good insonation conditions the ipsilateral TS with a signal
towardtheprobecanalsobeinsonated.Extracranialcompression of the IJV leads to an immediate reduction or even
cessationof flow in the ipsilateralTS and a flow increase in
the contralateral TS if a patent CoS is present (Fig. A2.84).
Reported detection rates vary between 30 % and 60 %. To
avoid direct insonation of the CoS inflow region we recommend placing the Doppler sample outside the midline.
To identify the SSS, the transducer direction is, starting
from the CoS or TS, slightly tilted superior. A signal adjacent to the calvarium, with flow direction toward the
probeisconsideredtobethedistalSSS(Fig. A2.85). The
maximal reported insonation rate is 50 %.
Normal values: Flow velocities: see Ta b l e A2.8 (p. 53).
Fig. A2.85 A Schematic drawing, sagittal plane. Note the distal part
of the SSS (shown in blue). B TCCS, transtemporal approach, upper
pontine to thalamic axial plane. Color-mode imaging of the distal
SSS demonstrated as a red-coded vessel segment. C CTA, midsagittal MIP. SSS segments accessible to duplex ultrasound are marked
(arrows) D Doppler spectrum analysis of the SSS (flow velocity: 11/
8 cm/s) with a flow towards the probe.
Fig. A2.86 MR T2-weighted image, axial (A)andcoronal(B)planes.
MR ce T1-weighted image, sagittal plane (C): Insonation field and
transducer position for examination of the SphS and SPS.
Sphenoparietal Sinus
Anatomic details: TheSpPScanbedividedintotwoparts.
In its first part it runs parallels to the middle meningeal
artery along the frontotemporal surface of the brain. Then
it turns and runs without an accompanying artery along
the lesser wing of the sphenoid bone toward the anterior
segment of the CS. In upto 60 % of cases it collects theblood
from the sylvian veins, and therefore from a considerable
part of the MCA territory.
Position and vessel identification: The SpPS can be insonated through the transtemporal bone window using the
upper pontine axial insonation plane (Fig. A2.86). We rec-
ommend to start identifying the hyperechogenic lesser
wing of the sphenoid bone in the conventional B-mode.
Then a small color window with a low PRF setting is placed
over this region. The SpPS, or alternatively, a strong sylvian
vein can then be identified as a venous signal along the
sphenoid bone, aiming toward the carotid siphon
(Fig. A2.87). The flowis directed away from the transducer.
A frequent finding is that the flow velocity increases the
closer the vessel gets to the CS. Venous flow velocities may
there reach up to 80 cm/s even in completely healthy individuals. Underlying reason for this phenomenon may be
a physiological venous narrowing at the entry into the CS
2 Vascular Anatomy and Structure of Ultrasound Examination48
Fig. A2.87 A Schematic drawing, axial MIP. Note the SphS along the
lesser wing of the sphenoid bone toward the CS (shown in blue).
B TCCS, transtemporal approach, upper pontine axial plane: Colormode imaging of a blue-coded prominent SphS. Note the commashaped carotid siphon. C CTA, axial MIP: Note the close spatial
relation of the distal SphS (arrows) and the carotid siphon (arrow)
D Doppler spectrum analysis of the SphS (flowvelocity: 19/16 cm/s)
with a flow away from the probe.
considerable amount of cerebral blood. It has a length of
approximately 2 cm in the anteroposterior direction, extending from the superior orbital fossa to the top of the
petrosal pyramid. It receives blood from the orbit via the
superior orbital veins, from the insular and opercular region as well as the temporal lobes via sylvian veins and
SpPS. Its main drainage follows the IPS into the superior
jugular bulb and via the basal emissaries (foramen lacerum, rotundum, ovale, and spinosum) toward the pterygoid plexus. However, it is also connected with the proximal SiS via the SPS.
Position and vessel identification: A critical point of analysis is the inflow and outflow region of the CS due to its
complex anatomy. A direct identification of the CS using
transcranial ultrasound is currently not possible. Venous
signals that are depicted within the region of the CS are
most probably feeding or draining vessel segments. Turbulent signals and high-flow velocities can frequently be
seen and should not be confounded with real stenoses or
increased flow caused by collateral venous function in a
presumed venoocclusive disorder.
Normal values: No normal values have been reported.
Fig. A2.88 A Schematic drawing, axial plane. Note the blue SPS
along its course at the upper edge of the petrous bone connecting
the CS with the SiS. B TCCS, transtemporal approach, upper pontine
axial plane. Color-mode imaging of ablue-coded SPS indicating flow
toward the SiS (arrows). Note the color signal of the carotid siphon
(single arrow). C CTA, axial MIP. Note the SPS originating from the CS
(arrows). D Doppler spectrum analysis of the SPS: Rare case with
prominent flow (flow velocity: 16/9 cm/s) with a flow away from the
probe.
(Valdueza et al.1998). Detection rates in individualswith a
patent transtemporal bone window reach up to 70 %.
Normal values: Flow velocities: see Ta b l e A2.8 (p. 53).
Cavernous Sinus (CS)
Anatomic details: The paired CS is a complex venous
structure responsible for collection and distribution of a
Superior Petrosal Sinus
Anatomic details: The SPS is in most cases a drainage
pathway for the CS toward the SiS, running along the
petrous bone from medial toward a lateral direction. However, depending on need, the flow direction might also be
toward the CS.
Position and vessel identification: The SPS can be visualized through the transtemporal bone window using the
axial upper pontine plane (Fig. A2.86).If detectable, often a
prominent vessel in projection of the C4/C5 segment of the
ICA is found (Fig. A2.88).Theflowdirectioncanbevariable—toward or away from the transducer—but is usually
away from the probe. Insonation rates have not been
reported.
Normal values: No normal values have been reported.
Inferior Petrosal Sinus
Anatomic details: The IPS is an important venous vessel
receiving blood from the posterior aspect of the CS. It runs
along the petroclival border to the ipsilateral IJV in most
cases or connects to the vertebral venous system. Its superior part is cone-shaped with a prominent width of
6–16mm. Distally, the IPS has a more tubular appearance
with a width of 2–7 mm. Right and left asymmetry is
frequent with a right-sided dominance in 75 % of cases
(Gebarski and Gebarski 1995).
Position and vessel identification: Systematic evaluations
have so far only been reported from TCD. Transforaminal
insonation yields a venous signal toward the probe at an
insonation depth of approximately 80–90mm, often simultaneously accompanied by the BA signal. The vessel
can also be visualized with TCCS through the upper and
lower transforaminal insonation plane using the same
identification criteria. Head rotation should be avoided
as artificial compression of the IJV may lead to underestimation or overestimation of velocities (Fig. A2.89). Reported TCD detection rates of at least one IPS reach 96 %
(Doepp et al. 1999).
Normal values: Flow velocities: see Ta b l e A2.8 (p. 53).
Special Venous Anatomy and Ultrasound Anatomy 49
Extracranial Veins
Internal Jugular Vein
Anatomic details: The IJVreceives its blood from the supe-
rior jugular bulb, which collects blood from the SiS and
frequently the IPS. Differences between the right and left
sides are common. Similar as to the TS, a right-sided dominance is found in about 50% of cases and a left-sided
dominance in 25%. Below the superior jugular bulb the
IJV runs initially behind and lateral of the ICA but then
circumscribes the ICA from lateral to finally lie in front of
the CCA. During its course the IJV collects blood from other
tributaries, the facial vein, the lingual vein, the superior
and medial thyroidal veins, and occasionally the occipital
vein (Hacker 1974). Before merging with the subclavian
vein to form the brachiocephalic vein it dilates to form the
inferior jugular bulb where the commonly paired jugular
valves are located (Fig. A2.73).
The IJVs are not the main drainage pathway of the intracranial blood in all subjects. In the supine body position,
the cerebral blood drains mainly via the IJV (defined as a
drainage of greater than two-thirds of the cerebral blood
flow via the IJV = “jugular drainer”)inonlyabout70%of
the general population (Fig.A2.90). The remaining 30 %
show a non-jugular type draining the blood predominantly via vertebral veins and deep neck veins (“neck
drainer”) or via the intraspinal venous system (“spinal
drainer”)(Fig. A2.91)(Doeppetal.2004).
Position and vessel identification: The IJV is insonated like
the CCA, ICA, and ECA recommendations in cross-sectional
and longitudinal insonation planes (Fig. A2.92,top).Longitudinal B-mode insonation in its caudal segment usually
permits the visualization of the inferior jugular bulb and
the jugular valve (Fig. A2.92, bottom). Further cranial, approximately at the level of the carotid bifurcation, the
merging facial vein can be seen in the cross-sectional
plane. In contrast with arteries, the patient has to be
insonated in a predefined body position; preferably a
head-straight, strictly supine position to get reliable and
reproducible results. Even slight turning of the head might
Fig. A2.89 A Schematic drawing adapted to the ultrasound image,
axial plane. Note the IPS along its course in the petroclival groove
toward the IJV (shown in blue). B TCCS, upper transforaminal ap-
proach. Color-mode imaging of a prominent long, red-coded IPS
segment lateral of the ipsilateral VA and BA. C MR contrast-enhanced T1-weighted sequence, coronal plane: Image of both IPS
(arrows). Note the widedistance to the BA in this example. However,
in case of a tortuous BA both vessels may be insonated simultaneously. D Doppler spectrum analysis of the IPS (flow velocity: 24/
19 cm/s) with a flow towards the probe.
Fig. A2.90 Example of a “jugular drainer” at rest in the supine body
position. A Contrast-enhanced 3D MRA, axial source image. Note
the dominant IJVon both sides (arrows). B, D Extracranial duplex, B-
mode image: Corresponding prominent IJV in the axial (B)and
longitudinal (D) insonation plane. C Doppler spectrum analysis
demonstrating a prominent monophasic flow. (Reproduced from
Doepp et al. 2004, Fig. 1, with kind permission of Springer Science
and Business Media).
lead to one-sided IJV compression with subsequent contralateral flow alteration. Elevation of the body leads to a
redistribution of cerebral venous outflow toward the vertebral venous system (Valdueza 2000). Head-down tilting
leads to an increased diameter of the IJV which is clinically
used to improve catheterization conditions for central
intravenous lines. Finally, insonation must be done under
normal breathing conditions. Increase in intrathoracic
pressure, e. g., by a Valsalva maneuver, leads to a raised
2 Vascular Anatomy and Structure of Ultrasound Examination50
Fig. A2.91 Example of a “non-jugular drainer” at rest in the supine
body position. A Contrast-enhanced 3D MRA, axial source image.
NoteaweaksignalintheleftIJV(arrow)andabsentrightIJV;
conversely, strong VVs (arrowheads) and deep neck veins (arrows)
with a right-sided dominance can be seen. B, D Extracranial duplex,
B-mode image, axial and longitudinal plane. Corresponding to the
MRAanopenleftIJVisseen.C Doppler spectrum analysis reveals
however an absent flow despite an open IJV lumen. (Reproduced
from Doepp et al. 2004, Fig. 2, with kind permission of Springer
Science and Business Media).
Fig. A2.93 Top: Extracranial duplex, cross-sectional B-mode image
of the IJV at rest (left) and under Valsalva maneuver (right). Note the
distinct enlargement of IJV lumen during Valsalva. Bottom: Doppler
spectrum with normal jugular flow (left). Flow reversal during Valsalva maneuver (start indicated by the arrow) instead of flow interruption in a patient with jugular valve incompetence (right).
IJV diameter and cessation of jugular flow. In up to 30 % of
the general population even a retrograde jugular flow is
observed during a Valsalva maneuver which is caused by
an IJV valve incompetence (Baehr et al. 2003) (Fig. A2.93).
Compression of a non-hypoplastic IJV with normal flow
will usually lead to a contralateral IJV increase, provided
that both TS are patent and they are connected via the
confluence of sinuses. In the normal population this occurs
in up to 63 % during right IJV compression and in up to 48 %
of left IJV compression (Doepp et al. 1998). The achievable
increase of flow velocity is between 15 % and 80 %.
Fig. A2.92 Top: Extracranial duplex, longitudinal plane: Doppler
spectrum analysis and color-mode image of the IJV (coded blue).
Note theadjacent red-coded CCA. Bottom:Serial B-mode image of a
jugular valve. A Open valve, B, C Valve closing.
Normal values: Flow profiles can vary considerably. Also,
absent flow may be observed even in a wide-open IJV. In
the elderly, biphasic profiles are more frequent than
monophasic flow patterns and a prominent flow modulation by the patients normal inspiration and expiration can
be observed. Flow velocities: see Ta b l e A2.8 (p. 53).
Vertebral Vein
Anatomic details: The VVs are one of four longitudinal
channels of the vertebral venous systems draining the
cerebral blood. For a detailed anatomic description, see
“General Venous Anatomy, Extracranial Venous Anatomy” (p.42). In contrast to the IJVs, the VVs do not collapse
on changing into the upright body position because of
their intraforaminal course. Similar to the IJV anatomy,
pairedvalvesarepresentintheproximalVV(Chouetal.
2002).
Position and vessel identification: For VV insonation we
recommend first visualizing the V2 segment of the VA.
Care must be taken to adjust the ultrasound system for
low flow velocities (low PRF) and to avoid IJV compression
during VV insonation. If the artery is identified, the VV is
usuallyseeninthemidcervicalregionmostlyasasingular
vessel accompanying the VA superiorly or as two vessels
which run parallel to the VA on either side with a flow
direction reverse to the VA toward the heart. Proximal to
its intraforaminal course the VV can be followed further
within the vicinity of the VA. Within its intraforaminal
course the VV can be insonated bilaterally in 62 % of cases
and unilaterally in 17 % of cases of a normal population.
Only 21 % of cases do not show any VV signal. Detection
rates decrease with increasing age (Hoffmann et al. 1999).
Bilateral compression of the IJV leads to a more than 100 %
flow increase in the VV which underlines its importance as
collateral pathway in IJV obstruction (Schreiber et al
2003d). Additional short intersegmental venous signals
can be often depicted especially in younger subjects. These
are the intervertebral veins, connecting the VV with, for
example, the anterior intraspinal venous system
(Fig. A2.94).
Normal values: Flow velocities: see Ta b l e A2.8 (p. 53).
Part A: Principles and Rules
Fig. A2.94 Extracranial duplex. Left top: Longitudinal B-mode VV
and VA image. VA diameter: 3.8 mm. VV diameter: 1.3 mm. Left
bottom: Corresponding color-modeimage. Note the intersegmental
veins connecting the VV with the anterior intraspinal segment and a
second VV medially of the VA. Right top: VA Doppler spectrum (flow
velocity: 63/25 cm/s). Right middle: VV Doppler spectrum (flow
velocity:24/21 cm/s).Right bottom:VV flow velocity increaseduring
ipsilateral IJV compression.
Special Venous Anatomy and Ultrasound Anatomy 51
Tab l e A2. 6 Reference values of extracranial arterial blood flow velocities
Vessel Systolic flow
CCA* 96 ± 25 26 ± 6Schöning 1994
ICA* 66± 16 26 ±6Schöning 1994
ECA main stem* 83 ± 17 17 ± 5Schöning 1994
STeA-ECA 57 ±2 Lauwerys 1997
OccA-ECA no systematic data available
V0-VA R*
V0-VA L*
V1-VA R*
V1-VA L*
V2-VA*
V2-VA R*
V2-VA L*
SA no systematic data available
Brachial artery* 81 ± 35± 1 Özcan 2006
*
angle-corrected
velocity ± SD
(cm/s)
66 ±18
61 ±17
60 ±14
58 ±10
48 ±10
49 ±11
51 ±10
Diastolic flow
velocity ± SD
(cm/s)
16 ±5
16 ±5
16 ±5
17 ±5
16 ±4
16 ±5
16 ±4
Reference
Kuhl 2000
Kuhl 2000
Schöning 1994
Kuhl 2000
2 Vascular Anatomy and Structure of Ultrasound Examination52
Tab l e A2 . 7 Reference values of intracranial arterial blood flow velocities
Vessel Systolic flow velocity ± SD
(cm/s) / Range ()
C6-ICA 53 ±14
(27–106)
Diastolic flow velocity ± SD
(cm/s) / Range ()
25 ±7
(13–48)
Reference
Own data
C5-ICA 49 ±16 19 ±7 Jurgita 2002
C3/C4-ICA 57 ±17
(31–105)
C1/C2-ICA 77 ±21
(33–140)
OA (transorbital) 35 ± 10
(15–67)
OA (transtemporal) 33± 9
(15–58)
M1-MCA* 108 ±18
(63–152)
A1-ACA* 91 ± 17
(53–
137)
V4-VA* 60 ± 16
(29–95)
25 ±8
(12–53)
34 ±10
(12–65)
14 ±5
(4–36)
11 ±4
(4–25)
48 ±8
(23–73)
40 ±8
(18–58)
27 ±9
(9–50)
Own data
Own data
Schreiber 2006
Schreiber 2006
Schöning 1993
Schöning 1993
Schöning 1992
PICA 48 ±526± 4 Kaps 1992a
BA transforaminal*
BA transforaminal
BA transtemporal
67 ±16
(35–114)
68 ±13
(41–104)
39 ±13
(18–77)
33 ±8
(18–48)
33 ±8
(20–56)
19 ±6
(9–38)
Schöning 1992
Own data
Own data
AICA no systematic data available
SCA 51 ±13
(39–104)
P1-PCA 60 ±14
(27–103)
P2-PCA 63 ±14
(37–123)
P3-PCA 63 ±12
(30–94)
ATA-PC A 26 ± 9
(12–60)
OTA-PCA 34 ± 9
(15–109)
POA-PCA 40± 14
(20–100)
CA-PCA 32± 12
(14–73)
24 ±7
(13–43)
28 ±9
(11–52)
30 ±10
(17–72)
30 ±8
(18–58)
12 ±4
(5–29)
16 ±5
(8–60)
21 ±8
(10–62)
16 ±6
(7–41)
Own data
Own data
Own data
Own data
Own data
Own data
Own data
Own data
PCoA 34 ± 14 - 37 ± 16 not reported Klötzsch 1996
*
angle-corrected
Special Venous Anatomy and Ultrasound Anatomy 53
Tab l e A2 . 8 Reference values of extracranial and intracranial venous blood flow velocities
Vessel Systolic flow velocity ± SD
(cm/s) / Range ()
Diastolic flow velocity ± SD
(cm/s) / Range ()
Reference
DMCV 9 ± 36± 2 Stolz 1999c
BVR 12 ± 49± 3 Stolz 1999c
ICV 7 ±25± 1 Stolz 1999c
VG 12 ± 48± 3 Stolz 1999c
StS
StS *
TS
TS *
12 ±5
26
(12–39)
14 ±6
32
(9–56)
9 ± 4
17
(7–27)
10 ±5
21
(5–38)
Stolz 1999c
Baumgartner 1997b
Stolz 1999c
Baumgartner 1997b
SSS 10 ±46±3 Stolz 1999c
SpPS
†‡
18 ±6
Valdueza 1 999a
(11–29)
SPS no systematic data available
†
IPS
20 ±9
Doepp 1999
(8–53)
IJV-R
IJV-L
VV-R
VV-L
*
angle-corrected
†
mean blood flow velocity
‡
data not representative
28 ±15
(5–77)
22 ±16
(0–67)
24 ±12
(8–66)
24 ±13
(5–81)
21 ±14
(0–70)
18 ±14
(0–59)
8 ± 8
(0–30)
8 ± 8
(0–30)
Pucheu 1994
Hoffmann 2000
54
3
Intracranial Hemodynamics and Functional Tests
Autoregulation ................................ 55
Testing of Autoregulation........................ 56
Neurovascular Coupling ........................ 56
Testing of Neurovascular Coupling................. 57
Metabolic Coupling ............................ 57
Other Tests to Assess Differences Between
the Right and Left Sides as Markers of Impaired
CollateralFunction.............................. 59
In contrast with many other organ systems, the human
brain has several characteristics that are of importance
when analyzing and interpreting cerebral perfusion. At
rest, the brain receives a high proportion of the total
cardiac output—in the order of 15–20 %. The global cerebral blood flow (CBF) in an adult amounts to 700–800 mL/
min, i. e., 13 mL/s or 55 mL/100 mg/min assuming a brain
weight of 1400 g. About of 75 % of the global CBF derives
from the internal carotid arteries (ICAs) and and the remaining 25 % from both vertebral arteries (VAs) (Schöning
199 4).
The ideal way to assess brain perfusion would be to
directly analyze CBF. However, conventional Doppler
flow velocity examination only generally permits flow
velocity analysis of proximal arterial or venous vessel segments. CBF and flow velocity are not equal but correlate
strongly with each other. A rising CBF causes rising blood
flow velocities, and a low CBF correlates with low blood
flow velocities. However, there are other factors that may
influence velocity more than CBF: Velocity tends to correlate with the size of a vessel’s vascular territory. For example, flow velocities in the MCA, which supplies the largest
cerebral territory, are higher than in the ACA and PCA but
peripheral CBF is similar in all. Flow velocities also depend
on the vessel size; in the case of local vessel narrowing,
velocity will rise. Other factors have more general effects.
Anemia leads to an generalized increase of flow velocities.
Flow velocities tend to decrease with increasing age,
which is attributed to brain atrophy and subsequent reduction of CBF with age. Under pathological conditions, for
example following ischemic stroke, reduced flow velocities may be found in the acute phase. In the reparative
phase, 1–3 weeks after the ischemic event, increased ve-
Parameters of Cerebral Hemodynamics .......... 60
Cerebral BloodFlow Velocity ..................... 60
Resistance Indices............................... 60
Cerebral BloodFlow............................. 60
Cerebral Circulation Time ........................ 61
Cerebral BloodVolume .......................... 62
locities can be seen in the hyperemic phase but the final
defect may, depending on its extent, again lead to a reduction of flow and velocity.
As brain tissue has virtually no energy reserves, changes
inperfusionleadtoanimmediatealterationinbrainfunction. Therefore, many regulatory processes (these are
listed and discussed below) exist to ensure a continuous
and constant blood supply. Probably more than any other
organ system, the brain needs to be constantly perfused
for optimal function. However, the heart, which is responsible for blood supply and blood drainage, is a pulsatile
pump. The solution to this problem are the arteries, which
with their elastic vessel walls are capable of storing a
considerable amount of blood during the systolic phase
that is then released into the circulation during diastole
(Windkessel function). This leads to an almost continuous
blood flow in the periphery.
For easier understanding of the flow pattern seen during
insonation of proximal arteries we will now introduce a
simple model (Fig. A3.1). A filled rain barrel is discharging
water through a rigid rain pipe. To imitate the pulsatile
action of the heart, a tap placed at the beginning of the pipe
is repetitively opened and closed. Flow analysis, in analogy
to ultrasound analysis of proximal arterial blood vessels, is
performed at the mid-segment of this pipe. The measured
flow is pulsatile witha high flow velocity presentwhen the
tap is open (systole) and no flow when the tap is closed
(diastole). If instead of a pipe an elastic water hose is used,
the flow profile will look different, i. e., more like the
arterial blood flow profile (Fig. A3.2). During the closing
phase of the tap, the elastic hose is causing a continuous
flow comparable with the arterial “windkessel” function. If
a second peripheral tap is added to the system, the micro-