Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_5776_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

30.08.2026

Размер:

53 Мб

Скачать

☆

<<< < Предыдущая 6 7 8 9 10 11 12 13 14 15 16 1718 / 5018 19 20 21 22 23 24 25 26 27 28 29 30 > Следующая >>>

149Arterial Pathology

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

Fig. A5.103 Top: 3D TOF-MRA, coronal MIP: Signal void in a prominent M2-MCA branch (arrow) indicating a high-grade M2 stenosis. Bottom: TCCS, transtemporal approach, axial midbrain plane with corresponding Doppler spectra showing a high-grade stenosis (non-angle-corrected ﬂ ow velocity 409/214 cm/s) in an insonation depth of 38 mm.

Fig. A5.104 TCCS , trans temp oral appr oach, axial m idbrain p lane. (A) Normal Doppler signal from the mid M1-MCA segment in a depth of 50 mm (ﬂ ow velocity: 73/39 cm/s). (B) Doppler signal from a prominent M2-MCA branch of the same case with turbulent ﬂ ow and raised ﬂ ow velocities in a depth of 43 mm (ﬂ ow velocity 225/122 cm/s) indicating a proximal M2-MCA branch stenosis.

A B

M1-MCA

M2-MCA

Fig. A5.105 (A) CTA axial MIP showing vessel narrowing in an M3MCA branch providing blood toward the angular artery (arrow). (B) Axial DWI MRI demonstrating acute ischemia in the posterior border zone indicating hemodynamic relevance of stenosis (arrow). (C,D) TCCS, transtemporal approach, axial upper midbrain plane. (C) Normal proximal M1-MCA ﬂ ow (98/36 cm/s). (D) Turbulent ﬂ ow and raised ﬂ ow velocity in the M3-MCA branch toward the angular artery (267/139 cm/s). Note the unfavorable insonation angle and reduced color signal intensity, implying an even higher true ﬂ ow velocity. (E) Marked poststenotic ﬂ ow pattern with delayed systolic ﬂ ow rise and reduced ﬂ ow velocity (28/15 cm/s) indicating a proxi- mal high-grade stenosis >70%.

and 3 and COGIF 3) (Fig. A5.109 and Fig. A5.110). Some- times the ﬂ ow signal in the M1 MCA can be followed in 1-mm steps up to the vessel occlusion. As the lenticulostriate perforators are normally separated into a proximal and distal bundle, TCCS can document the loss of ﬂ ow in the more distal vessel (Fig. A5.111; see also Video

A5.14).

The assessment of ﬂ ow velocities in the A1-ACA and PCA segments is of paramount importance, as raised ﬂ ow veloc- ities in these vessels indicate ﬂ ow diversion with leptome- ningeal ﬂ ow toward the MCA territory. They therefore in- directly conﬁ rm a major proximal obstruction of the MCA.

Fig. A5.106 (A,C) CTA, axial MIP, 90° counterclockwise rotated to correspond with TCCS image. (B,D) TCCS, transtemporal approach, axial midbrain plane, color-mode. (A) Left M1-MCA occlu- sion with absent contrast ﬁ lling (arrows). (B) Corresponding TCCS color-mode image. Absent MCA color signal. A slight B-mode hyper echoic area indicates MCA occlusion (“hyperechoic media sign”) (arrows). Marked color-ﬂ ow signal (arrow). (C) CTA of the same patient. Note the present contralateral MCA signal (arrow). (D) Corresponding TCCS color-mode image of the right side with normal MCA and PCA (arrow).

In case of a well-developed early temporal branch this vessel may compensate for a large part of the original MCA territory. This may lead to almost normal-appearing proximal M1-MCA Doppler spectra, despite the presence of a midpart or distal M1-MCA occlusion, and higher ﬂ ow compared with cases in which only the perforators remain perfused. False-positive ﬁ ndings may occur if the early tem- poral branch is confounded with the M1-MCA segment itself. To avoid this mistake, we recommend careful B-mode insonation of the midbrain plane to visualize the hyperechoic structure of the lateral ﬁ ssure which contains the

150 5 Vascular Pathology

Fig. A5.107 (A) 3D TOF-MRA, axial MIP 90° counterclockwise rotated to correspond with TCCS image revealing a proximal M1-MCA occlusion (yellow circle). (B) TCCS, transtemporal approach, axial midbrain plane, color-mode. M1-MCA occlusion with absent color signal (yellow circle). Note the prominent ipsilateral and also partly contralateral PCA (arrows) as well as the prominent contralateral M1-MCA and A1-ACA (arrowheads).

Fig. A5.108 Left: CCT, axial plane. Not the dense media sign indicating M1-MCA occlusion (arrow). Right: TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. To p: Left M1-MCA occlusion with absent arterial color and Doppler signal. Only a blue-coded vessel signal with a flow away from the probe and a venous waveform—the deep middle cerebral vein (11/9 cm/s) is detectable in a depth of 56 mm. Bottom: Prominent nonturbulent ipsilateral A1-ACA flow in a depth of 62 mm with a flow velocity of 148/66 cm/s confirming collateral flow activation.

Fig. A5.110 Top: 3D TOF-MRA, coronal MIP: Long segmental signal loss in the midpart of the M1-MCA consistent with occlusion (arrow). Note the length of the unaﬀ ected M1-MCA. Middle and

bottom: TCCS, transtemporal approach, axial midbrain plane with

Fig. A5.109 Left: DSA, selective right ICA injection,

p o s t e r o a n t e r i o r v i e w : M 1 - M C A o c c l u s i o n ( a r r o w ) d i s t a l o f t h e l e n t i c u l o s t r i a t e p e r f o r a t o r s . N o t e t h a t t h e b a s a l g a n g l i a a r e n i c e l y p e r f u s e d ( a r r o w h e a d s ) . Right: TCCS, transtemporal approach, axial midbrain plane with corresponding Doppler spectra. Top: Reduced flow velocity in the proximal M1-MCA (32/12 cm/s) with normal PI. Middle: Increased nonturbulent flow in the A1-ACA (105/46 cm/s). Bottom: Normal flow signal in the proximal PCA (69/31 cm/s) indicating collateral leptomeningeal flow mainly via the ipsilateral A1-ACA.

corresponding Doppler spectra showing a reduced ﬂ ow velocity in the proximal M1-MCA (35/15 cm/s) in a depth of 51 mm with normal PI (middle) and no real ﬂ ow but artifacts in the distal M1-MCA at 47 mm assumed to be vessel wall vibrations (bottom). TCCS ﬁ nd- ings indicate a midpart M1-MCA occlusion.

horizontal segment of the MCA. After an optimal B-mode image is achieved the color mode is started, which will then visualize the M1 segment if present (Fig. A5.112). Starting with color mode and neglecting the insonation planes are usually the reasons for mistaking the prominent temporal branch at the upper pontine plane for the main stem of the MCA (Fig. A5.113 and Fig. A5.114). Also useful is to look for a color gap which should not be present during a thorough step-by-step vessel investigation. Although following the color and Doppler signal can be a challenge in patients with

151Arterial Pathology

44 mm

42 mm

40 mm

38 mm

Fig. A5.111 Left: DSA, selective left ICA injection, posteroanterior view: Distal M1-MCA occlusion (arrow) distally at least of the medial bundle of the lenticulostriate perforators with the basal ganglia partly perfused. Note the leptomeningeal collateral ﬂ ow via the ACA (arrowheads). Right: TCCS, transtemporal approach, axial midbrain plane, Doppler spectra showing the stepwise loss of ﬂ ow following the M1-MCA from a depth of 44 mm in which a highly pulsatile signal of low ﬂ ow velocity (30/2 cm/s) is detectable to a depth of 38 mm in which only a systolic signal (19 cm/s) can be seen. The ipsilateral A1-ACA revealed a compensatory increased ﬂ ow velocity of 103/20 cm/s (not shown).

Fig. A5.112 Midpart M1-MCA occlusion with a prominent early temporal M1 branch. (A,B) TCCS, transtemporal approach, ax- ial midbrain plane, B-mode. Note that the hyperechoic lateral fissure holding the M1-MCA segment is excellent visible (yellow circle). (C,D) TCCS, transtemporal approach, axial midbrain plane, color-mode. Normal color-mode signal of the MCA main stem on the unaffected side (C), missing main stem color signal on the affected side (D). (E,F) CTA, axial MIP, rotated 90° counterclockwise to correspond with TCCS image shows a normal anatomy on the unaffected side (E) and a missing M1 segment contralateral (F).

Fig. A5.113 Midpart M1-MCA occlusion with a prominent early temporal M1 branch. Left: DSA, selective ICA injection, posteroanterior view: Distal M1-MCA occlusion (arrowheads) with a strong early temporal branch (blue circle). Right, top: TCCS, transtemporal approach, axial midbrain plane, color-mode. Note the missing M1 MCA color signal (arrowheads). The distant color signal corresponds to the ascending segment of the early temporal branch (red circle, also marked on the DSA). Right, bottom: TCCS, transtemporal approach, axial upper pontine plane, color-mode. Note the visible red-coded vessel corresponding to the prominent early temporal branch (blue circle, also marked on the DSA). The visualization of the carotid siphon (arrow) facilitates correct determination of insonation plane.

Fig. A5.114 Midpart M1-MCA occlusion with a prominent early temporal M1 branch. TCCS, transtemporal approach, axial midbrain plane (A,C,D) and upper pontine plane (B) with corresponding Doppler spectra. (A,C) Unaﬀ ected side showing normal ﬂ ow velocities in the M1-MCA (91/25 cm/s) and A1-ACA (63/19 cm/s). (B,D) Pathologic side with marked ﬂ ow in an early MCA tempo- ral branch (69/29 cm/s) to compensate for the distally located MCA occlusion and raised A1-ACA ﬂ ow velocity (100/40 cm/s), both indicating leptomeningeal collateral support. Carotid siphon ( a r r o w ) c o n ﬁ rms exact determination of the upper pontine i n s o n a t i o n p l a n e a n d p r e v e n t s c o n f o u n d i n g o f t h e t e m p o r a l branch with the main stem MCA.

severe elongations, an obvious color gap may help to distinguish a tortuosity from a distal M1 occlusion. Finally, the system settings should be adjusted (low PRF, increased color gain) in order not to diagnose occlusion instead of a near-occlusion and not to miss a low ﬂ ow pattern in distal occlusion (Fig. A5.115). Nonetheless the ultrasound analysis of ﬂ ow

distribution and the assessment of vessel pathology in this area may be diﬃ cult. More distally located MCA pathology, such as an M2-MCA branch occlusion of one or more M2 branches, leads to a reduced proximal ﬂ ow which might be detected with ultrasound because of lower velocities in comparison to the contralateral homologous vessel segment

152 5 Vascular Pathology

Fig. A5.115 M1-MCA occlusion. TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. (A) Using standard PRF and color gain TCCS settings the contralateral MCA main stem, both ACAs, and both PCAs are easily depicted while the ipsilateral MCA signal is missing. The above vessel visualization and the visible proximal MCA vessel sheath within the lateral ﬁ ssure (yellow circle) conﬁ rm the correct insona- tion plane—an occlusion may be diagnosed. (B) PRF reduction and increase of color gain yields a positive proximal MCA color signal with a reduced ﬂ ow signal on Doppler spectra analysis (32/12 cm/s) (C)—i.e., the diagnosis of midpart or distal M1-MCA occlusion.

(Fig. A5.116). Flow velocity data to distinguish the diﬀ erent MCA occlusion patterns are not well established. One TCCS study correlated ultrasound data with DSA and analyzed end-diastolic ﬂ ow velocities in MCA main stem and MCA branch occlusions. An end-diastolic ﬂ ow velocity <26 cm/s was suspicious for a main stem or branch occlusion. An end-diastolic velocity ratio (dividing the velocity of the unaffected side by that of the aﬀ ected side) of >2.5 was indicative of a main stem occlusion (Ogata et al 2005). Such threshold values might be helpful, but they should be used cautiously as just one occluded M2-MCA branch will not automatically cause any detectable ﬂ ow alterations in the proximal vessel segments—mainly because of the compensation via the patent and now even more perfused other M2 branch(es) via leptomeningeal anastomoses. (For further reading, see also Case 13. For further details about leptomeningeal collateral ﬂ ow, see “Intracranial Collateral Pathways in ICA Occlusive Processes” below). The hemodynamic eﬀ ects of MCA occlu- sion in relation to its location are presented in Fig. A5.98. For further details about MCA occlusion see Case 10, Case 17, Case 25, and Case 39, and for MCA occlusion and early temporal branch see Case 22.

ACA Stenosis

For evaluation of the A1-ACA segment, diﬀ erences be- tween the right and left sides cannot be used as criteria of stenosis as physiologic variations in diameter are a frequent ﬁ nding (for ACA anatomy, see Chapter 2, “An- terior Cerebral Artery” under “Special Arterial Anatomy and Ultrasound Anatomy”). Furthermore, a unilateral A1-ACA stenosis may not cause raised ﬂ ow veloci- ties because of a suﬃ cient collateral compensation via the contralateral A1-ACA segment and the ACoA and may therefore be diﬃ cult to detect (Fig. A5.117). In any other instance A1-ACA stenoses may also be

Fig. A5.116 Left: 3D TOF-MRA, coronal MIP. Right: TCCS, tran- stemporal approach, axial midbrain plane with corresponding Doppler spectra. Top : Normal TOF-MRA ﬁ ndings for the right M1- MCA and both M2-MCA branches and normal M1-MCA Doppler spectrum ﬁ ndings: 131/62 cm/s. Bottom: TOF-MRA demonstrat- ing M2-MCA branch occlusion on follow-up examination (arrows). M1-MCA Doppler spectrum shows a correspondingly reduced ﬂ ow velocity of 58/31 cm/s.

A BC

Fig. A5.117 Proximal A1-ACA. (A) DSA, selective right ICA injec- tion, posteroanterior view revealing a proximal A1-ACA stenosis (arrow). Considering the weak contrast in the A2-ACA a hemodynamically relevant stenosis can be assumed. (D) 3D TOF-MR A, coronal MIP confirms proximal A1-ACA stenosis (arrow). The flow gap suggests high-grade stenosis. The prominent contralateral A 1 - A C A a n d t h e e q u a l A 2 - A C A s i g n a l i n t e n s i t y s u g g e s t i p s i l a t e r al A1-ACA hypoplasia. (B,C) TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. Note a turbulent A1-ACA flow with a peak systolic flow velocity of 116 cm/s—just at the border of the Baumgartner classification of a <50% stenosis. No angle correction is needed as the vessel runs directly in line with the insonation beam. Flow of both A2-ACA segments was normal (not shown), as both are provided with blood via the dominant contralateral A1-ACA. In summary, TCCS would have underdiagnosed this A1-ACA stenosis because of its hypoplastic nature.

e v a l u a t e d a c c o r d i n g t o ﬂ ow velocity and the presence of turbulences (Fig. A5.118; see also Fig. A5.92). Using modern ultrasound systems, distal assessment of the A2-ACA segment is possible in some cases, allowing the

153Arterial Pathology

Fig. A5.118 Top: 3D TOF-MRA, coronal MIP demonstrating a distal A1-ACA stenosis in a dominant ACA (arrow). The missing ﬂ ow gap suggests a nonhemodynamically relevant stenosis. Bottom: TCCS , tra nstem pora l app roach, a xial midb rain plane, colo r-mo de and corresponding Doppler spectra. Note a turbulent A1-ACA ﬂ ow (175/80 cm/s) consistent with a >50% stenosis according to the Baumgartner criteria. The ipsilateral A2-ACA ﬂ ow was normal (not shown), therefore TCCS diagnosis is also a nonhemodynamically relevant stenosis.

a s s e s s m e n t o f p o s t s t e n o t i c ﬂ ow alterations or stenoses of the A2-ACA segment itself (Fig. A5.119).

ACA Occlusion

The variability of ACA anatomy may also hinder a clear diﬀ erentiation between aplasia and occlusion. In such cases all available clinical information should be taken into account. If the patient has an acute leg paresis contralateral to the missing A1-ACA segment and ipsilateral MCA and PCA ﬂ ow velocities are raised (indicating leptomeningeal collateralization) then A1-ACA steno-occlusive pathology seems likely. Direct TCCS assessment of A2-ACA occlusions has not yet been reported.

Intracranial Posterior Circulation

PCA Stenosis

Recent CTA studies have shown that stenoses of the PCA are common ﬁ ndings in stroke patients, accounting for about one-quarter of all intracranial lesions (Homburg et al 2011, Ovesen et al 2013). PCA stenoses are graded following the same principles as in MCA pathology by analyzing the magnitude of observed ﬂ ow velocities, the presence of tur- bulence, and indirect signs of hemodynamic compromise (Fig. A5.92). As the P2- and P3-PCA segments are usually symmetrically developed, diﬀ erences between the right and left sides can also be considered in these segments. Although there are no extensive data regarding these differences, as with MCA pathology the same criteria of at least 30 cm/s ﬂ ow velocity diﬀ erence as a cut-oﬀ can be used to diﬀ erentiate between physiologic and pathologic diﬀ erences, provided that the insonation angles are com- parable. Turbulent ﬂ ow may further contribute to diagnos- ing a stenosis. An asymmetry analysis cannot be applied to the P1-PCA segment because of the rather frequently seen

Fig. A5.119 Left: 3D TOF-MRA, coronal MIP, 90° counterclockwise rotated to correspond with the ultrasound image demonstrating a proximal A2-ACA stenosis of the dominant ACA (arrow). Note that no ACoA can be detected. Right: TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. Top: Normal A1-ACA ﬂ ow signal on at the aﬀ ected side (51/15 cm/s). Middle: Circumscribed velocity rise in the proximal A2-ACA of 88/35 cm/s (angle-corrected 158/71 cm/s), corresponding to a >50% stenosis according to the Baumgartner criteria. Bottom: Contralateral A2-ACA signal approached from the same insonation side: 48/21 cm/s.

variation of a fetal-type PCA (see also “Fetal-type Posterior Cerebral Artery” under “Collateral Pathways” below). A P1PCA stenosis in a hypoplastic P1 segment may not result in a pathologic ﬂ ow velocity rise, but insonation may rather re- veal pseudo-normalized ﬂ ow velocities. In our experience, the most common location of PCA stenosis is in the proximal P2 segment (Fig. A5.120). At this site the SCA may be confused with the PCA and careful TCCS analysis is required (Fig. A5.121 and Fig. A5.122). Furthermore, indirect hemo- dynamic criteria also apply to the PCA. A hemodynamically relevant stenosis will cause a distal poststenotic ﬂ ow pat- tern (Fig. A5.123). PCA stenoses may also be located more distally, i.e., in the distal P2-PCA or P3-PCA (Fig. A5.124 and Fig. A5.125). Findings of bilateral or tandem stenoses are not infrequent and therefore careful examination of all available segments of the PCA is recommended, particularly in PCA stroke (Fig. A5.126). PCA stenosis may also be detectable in branches of the main stem (see also Video

A5.15). For

further discussion on PCA stenosis, see Case 6.

PCA Occlusion

Again, the guidelines for MCA occlusion can also be applied in PCA occlusion. Direct sign of a proximal PCA o c c l u s i o n i s a n a b s e n t c o l o r s i g n a l . I n t h i s c a s e t h e S C A may be seen with a color and Doppler signal similar to the PCA. However, as the proximal SCA is usually seen in the upper pontine plane and not in the midbrain plane, diﬀ er- entiating between the two vessels should be feasible (Fig. A5.127). Doppler spectrum analysis may show an absent ﬂ ow signal. In more distal occlusion a large variety of ﬂ ow signals and velocities may be observed because of the high variability of the cortical PCA branches. In occlusion of the P3-PCA segment a dampened ﬂ ow signal (corresponding to TIBI and COGIF grades 3) may be observed proximally (Fig. A5.128). A P1-PCA occlusion may escape detection if

154 5 Vascular Pathology

Fig. A5.120 Proximal P2-PCA stenosis. (A) DSA, selective VA in- jection, posteroanterior view revealing no real pathology; a mild proximal P2-PCA stenosis was postulated retrospectively (arrow). (B,C) TCCS, transtemporal approach, axial midbrain plane, colormode and corresponding Doppler spectra. Note the turbulent ﬂ ow in the P2-PCA (depth 59 mm, non-angle-corrected ﬂ ow ve- locity 170/87 cm/s) deﬁ ning a stenosis >50% according to the Baumgartner classiﬁ cation. This case illustrates that invasive an- giography is prone to underestimate a stenosis, inherent to the choice of a single two-dimensional projection for the diameter reduction measurement.

Fig. A5.121 (A) 3D TOF-MRA, axial MIP demonstrating a proxi- mal P2-PCA stenosis (arrow). (B) TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. Note the turbulent flow in the P1/P2-PCA transition (depth 61 mm, flow velocity of 222/89 cm/s) consistent with a >50% stenosis according to the Baumgartner classification. (C) TCCS, transtemporal approach, axial slight caudal probe tilting reveals the SCA signal with normal flow parameters of 46/17 cm/s instead of the PCA.

Fig. A5.122 (A) 3D TOF-MRA, axial MIP demonstrating a proxi- mal P2-PCA stenosis (arrow) and normal SCA (arrowhead). (B,C) TCCS , transt emporal ap proach, ax ial midbrain plane, colo r-mode and corresponding Doppler spectra. Note the turbulent ﬂ ow in the proximal P2-PCA (depth 59 mm, ﬂ ow velocity 242/124 cm/s) consistent with a >50% stenosis according to the Baumgartner classiﬁ cation (B). The SCA is visible in the same insonation plane, dorsal to the PCA, showing a normal ﬂ ow signal and velocities of 53/18 cm/s (C).

a large PCoA is present as this constellation appears to be a physiologic fetal-type PCA. However, in case of an occluded P1-PCA with a normal lumen, turbulent ﬂ ow and a compensatory increased ﬂ ow velocity with a ﬂ ow toward the posterior circulation should be seen in the PCoA. A further important diagnostic pitfall can be caused by the SCA—a vessel which may show ﬂ ow velocities similar to a normally developed PCA and runs parallel to the PCA

Fig. A5.123 (A) 3D TOF-MRA, axial MIP demonstrating a proximal P2-PCA stenosis with a short signal gap indicating a hemodynamically relevant stenosis (arrow). (B) TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. Note the turbulent ﬂ ow in the proximal P2-PCA (depth 62 mm, ﬂ ow velocity 298/151 cm/s) consistent with a >50% stenosis according to the Baumgar tner classiﬁ cation. (C,D) TCCS, transtempo- ral approach, axial thalamic plane, color-mode and corresponding Doppler spectra of the distal P2-PCA of both sides. Despite velocities being similar, the side with a stenosis reveals a poststenotic

ﬂ ow pattern (C) in contrast to the side without stenosis (D), con- ﬁ rming the hemodynamic relevance of the stenosis.

in its proximal and distal course. In elderly patients with e l o n g a t e d a r t e r i e s i n w h o m t h e S C A m i g h t a l s o b e d e t e c t ed in the midbrain plane, a SCA/PCA diﬀ erentiation can also be diﬃ cult along the more distal segments. Arterial segments with projection into the thalamic plane, however, can only be allocated to the distal P2-PCA or the basal vein of Rosenthal (BVR). In a patient with PCA infarction, arterial signals in the midbrain plane should therefore not

155Arterial Pathology

Fig. A5.124 (A) 3D TOF-MRA, axial MIP demonstrating a distal P2PCA stenosis without signal gap indicating a nonhemodynamically relevant stenosis (arrow). (B,C) TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. Note the turbulent ﬂ ow in the distal P2-PCA (depth 61 mm, ﬂ ow velocity 170/65 cm/s) consistent with a >50% stenosis according to the Baumgartner classiﬁ cation.

Fig. A5.125 (A) 3D TOF-MRA, axial MIP demonstrating a proximal P3-PCA stenosis (arrow). (B,C) TCCS, transtemporal approach, axial thalamic plane, color-mode and corresponding Doppler spectra. Note the turbulent ﬂ ow in the proximal P3-PCA (depth 64 mm, ﬂ ow velocity 127/58 cm/s). The distal vessel segments had a normal ﬂ ow pattern. Despite the mild signal gap seen on MRA, the most likely diagnosis was considered to be a <50% stenosis according to the Baumgartner classiﬁ cation.

Fig. A5.126 PCA tandem stenoses. Top , m id dle : 3D TOF-MRA, axial MIP, rotated 90° counterclockwise to correspond with the ultrasound image. Left and right: TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra. Left: Proximal P2-PCA stenosis (depth 59 mm, ﬂ ow veloc- ity 160/61 cm/s) consistent with a >50% stenosis according to the Baumgartner classiﬁ cation. Right: Distal P2-PCA stenosis (depth 58 mm, ﬂ ow velocity 105/36 cm/s) indicating a stenosis grade <50%. The grade may be underestimated because of the concomitant proximal stenosis. Note a prominent anterior temporal artery (arrow).

be automatically attributed to the PCA. However, in the presence of a venous signal in the midbrain plane (ﬂ ow direction toward the probe) and missing proximal PCA signal or in the presence of a venous signal (ﬂ ow away from the probe) in the thalamic plane and missing distal PCA signal, a proximal or distal PCA main stem occlusion can be assumed (Fig. A5.129). Again, consideration of the B-mode insonation planes is of special importance. In good insonation conditions, a single proximal midbrain plane arterial signal with a normal ﬂ ow toward the probe

Fig. A5.127 Proximal PCA occlusion. (A) 3D TOF-MRA, axial MIP, rotated 90° counterclockwise to correspond with the ultrasound image. Only a short PCA segment is visualized (small arrow). Instead of the PCA the SCA can be followed (arrowhead). Note the carotid siphon (large arrow). (B,C) TCCS, transtemporal approach, axial upper pontine plane, color-mode and corresponding Doppler spectra revealing the SCA (arrowhead) in its course in the upper pontine plane with a normal ﬂ ow (velocity 55/22 cm/s) not distin- guishable from a normal PCA ﬂ ow signal. Note that the concomi- tantly insonated carotid siphon (large arrow) helps to identify the upper pontine plane and to assure the SCA.

in an angiographically known PCA occlusion will probably be allocated to the SCA. In case of low ﬂ ow velocities in an identical sample volume position, a distal PCA occlusion, e.g., of the relevant cortical branch, should be considered (Fig. A5.130).

Otherwise, raised ﬂ ow velocities within the A1-ACA or M1-MCA segments indicating leptomeningeal ﬂ ow to the PCA territory may be present. Such a ﬂ ow diversion may also occur with P2- and P3-PCA occlusions. Increased ﬂ ow velocities may then be detected ipsilaterally in the

156 5 Vascular Pathology

P2/3-PCA / BVR L

P2/3-PCA R

BVR R

Fig. A5.128 TCCS, transtemporal a pproach, axial midb rain/ thalamic plane. (A) Normal color-mode and Doppler spectrum of the proximal left P2/3-PCA which is accompanied by the BVR (flow velocity artery 81/29 cm/s, vein 20/10 cm/s). (B) Contralateral right PCA Doppler spectrum with markedly reduced flow velocity (22/13 cm/s) indicating a distal PCA occlusion. (C) Signal of the right basal vein of Rosenthal located lateral to the PCA (flow velocity: 20/10 cm/s).

Fig. A5.129 Proximal PCA occlusion. (A) 3D TOF-MRA, axial MIP, rotated 90° counterclockwise to correspond with the ultrasound image. Missing PCA signal. The remaining weak signal in projection of the PCA corresponds to the SCA (arrows). Note the prominent MCA signal intensity (arrowhead) indicating leptomeningeal collateral ﬂ ow. (B,C) TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra revealing proximal BVR with ﬂ ow toward the probe (B) and the distal SCA with a ﬂ ow away from the probe (C, ﬂ ow velocity 40/16 cm/s). (D) TCCS, tran- stemporal approach, axial thalamic plane, color-mode and corresponding Doppler spectra showing the distal BVR with a normal ﬂ ow signal but no accompanying arterial PCA signal.

Fig. A5.130 (A) 3D TOF-MRA, axial MIP, suggestive for a PCA occlusion at its middle P2 segment. (B) Raw TOF-MRA data reveal a persisting distal P3-PCA segment, presumably with a reduced ﬂ ow. (C,D) TCCS, transtemporal approach, axial thalamic plane, colormode and corresponding Doppler spectra revealing distal P2 and beginning of the P3-PCA segment with a reduced ﬂ ow velocity (35/17 cm/s) indicative of a more distal vessel occlusion.

proximal cortical PCA branches caused by a raised leptomeningeal collateral ﬂ ow. Distal PCA branch occlusion might not have any hemodynamic eﬀ ect and is therefore often overlooked.

SCA Stenosis

A major stenosis may be detected in the cerebellar arteries in corresponding strokes. An SCA stenosis can be diagnosed with certainty if the PCA is concomitantly vis-

Fig. A5.131 (A) DSA, selective VA injection, posteroanterior view revealing a proximal SCA stenosis (arrowhead). Note the incomplete fetal-type PCA with P1-PCA hypoplasia (arrow). (B–D) TCCS, transtemporal approach, posterior coronal plane, color-mode and corresponding Doppler spectra. Normal ﬂ ow signal in the proximal P2-PCA (B). Turbulent ﬂ ow and increased velocities of 94/23 cm/s at the SCA origin (C). The distal SCA segment reveals a normal ﬂ ow signal and velocities (46/8 cm/s) (D).

ualized with a normal ﬂ ow signal using the coronal or axial planes (Fig. A5.131).

BA Stenosis

The BA is a typical site for intracranial stenoses (Kurre et al 2010). A combined approach allows assessment of the BA over its full length, provided that the insonation conditions are good: a transforaminal approach for at least the

157Arterial Pathology

CBA

Fig. A5.132 (A) 3D TOF-MRA, coronal MIP, revealing a proximal BA stenosis (arrow). (B) 3D TOF-MRA, same coronal MIP, rotated 180° to correspond with the ultrasound image. (C) TCCS, transforaminal approach, color-mode and corresponding Doppler spectra: Normal ﬂ ow with 87/32 cm/s at the BA origin (depth 76 mm) (D) Aliasing in the color mode and turbulent ﬂ ow with increased ﬂ ow velocities of 229/84 cm/s in the BA (depth 82 mm) indicating a >50% stenosis. No poststenotic ﬂ ow pattern was seen (not shown).

Fig. A5.133 (A) 3D TOF-MRA, coronal MIP, revealing a signal gap at the VAs conﬂ uence indicating a high-grade stenosis of the distal VAs or the BA origin or both (arrow). (B,C) TCCS, transforaminal approach, color-mode and corresponding Doppler spectra revealing a disturbed ﬂ ow with increased ﬂ ow velocities (224/114 cm/s) relating to a >50% stenosis, probably of the proximal BA. A mild poststenotic ﬂ ow pattern was seen in the distal BA (not shown). Note the distal loop of the V3-VA on both sides (arrowheads).

PCA

SCA

Fig. A5.134 (A) 3D TOF-MRA, coronal MIP. Midpart BA stenosis (ar- row). (B) TCCS, transforaminal approach, color-mode and corresponding Doppler spectra with detection of a stenotic ﬂ ow signal at 80 mm depth, 210/95 cm/s. Note the oscillation eﬀ ect on tapping of the VA at the atlas arch. (C) TCCS, transtemporal approach, posterior coronal plane, color-mode and corresponding Doppler spectra conﬁ rming the midpart BA stenosis (angle-corrected ﬂ ow velocity 226/98 cm/s).

proximal two-thirds of the BA and a coronal transtemporal insonation approach for at least the distal one-third. Echo contrast agents facilitate the detection of BA stenoses (Tateishi et al 2008). Velocity cut-oﬀ values for >50% and <50% stenosis are given in Fig. A5.92. Atherosclerotic BA stenoses often aﬀ ect the proximal and mid segments of the BA and therefore the transforaminal approach should always be used (Fig. A5.132). As stenoses frequently begin at the conﬂ uence of both VAs it is often diﬃ cult to deﬁ ne where the main point of the lesion is (Fig. A5.133). In cases with impaired transforaminal insonation conditions, the transtemporal approach may be of help at least for the detection of distal and mid BA stenoses (Fig. A5.134 and Fig. A5.135). Detection of indirect hemodynamic signs

Fig. A5.135 (A) 3D TOF-MRA, sagittal MIP. Distal BA stenosis (arrow). (B) TCCS, transtemporal approach, posterior coronal plane, color-mode and corresponding Doppler spectra with detection of a stenotic ﬂ ow signal (ﬂ ow velocity 253/133 cm/s). (C) TCCS, trans- temporal approach, axial insonation, lower pontine plane, colormode and corresponding Doppler spectra revealing the stenosis in a transtemporal axial plane (ﬂ ow velocity 226/118 cm/s).

depends on the location and grade of the stenosis as well as on the presence of a PCoA. Prestenotic ﬂ ow alterations are absent in distal stenosis but may be present in both VAs in proximal high-grade BA stenosis (see also “BA Occlusion” below). A poststenotic ﬂ ow pattern of varying extent in the distal BA or in the PCA with or without a functional stenosis in the PCoA may be observed (Fig. A5.136).

BA Occlusion

Occlusions of the BA can be diﬃ cult to assess and diag- nostic certainty depends on the site of the occlusion. As with stenoses, the location of an occlusion should be differentiated into proximal, mid, or distal. In general, if TCD

158 5 Vascular Pathology

CBA

Fig. A5.136 (A) DSA, selective VA injection, posteroanterior view, rotated 180° to correspond with the ultrasound image revealing a proximal BA stenosis estimated at 60% (arrow). (B) 3D TOF-MRA, coronal view, rotated 180° to correspond with the ultrasound image shows a signal gap, indicative of a high-grade stenosis (>70%). (C,E) TCCS, transforaminal approach, color-mode and corresponding Doppler spectra conﬁ rming a proximal BA stenosis with a high ﬂ ow velocity of 286/74 cm/s and musical murmurs, indicative of a hemodynamically relevant stenosis. The distal BA segments were not detectable by ultrasound. (D) TCCS, transtemporal approach, axial insonation, midbrain plane, color-mode and corresponding Doppler spectra showing the anterior temporal artery (ﬂ ow toward the probe) and the distal P2-PCA (ﬂ ow away from the probe) with a mild poststenotic ﬂ ow pattern conﬁ rming the hemodynamically relevance of the BA stenosis, missed by the DSA assessment.

V2-VA LV2-VA R

Fig. A5.137 Middle: Cont rast-en hance d MRA, coron al vie w, shows a right-sided dominant VA ending in a PICA and a missing BA signal (arrows) indicative of a proximal BA occlusion. Left and right: Extracranial duplex, V2-VA insonation in the longitudinal insonation plane, color-mode imaging and corresponding Doppler spectra. Both V2-VAs had normal diameter (right 4.5 mm, left 3.2 mm) and high pulsatile ﬂ ow signals (right 44/2 cm/s, left 33/7 cm/s) compat- ible with a VA occlusive lesion distal from the PICA origin or compatible with a relevant proximal BA pathology.

CBA

Fig. A5.138 Proximal BA occlusion. (A) 3D TOF-MRA, axial MIP, rotated 90° counterclockwise to correspond with the ultrasound image. Note the marked PCoA (arrow) and a short P1-PCA (arrowhead). (B,C) TCCS, transtemporal approach, axial midbrain plane, color-mode and corresponding Doppler spectra revealing PCoA with a turbulent ﬂ ow toward the posterior circulation and increased ﬂ ow velocity considered to be a functional stenosis (ﬂ ow velocity 99/31 cm/s). (D) 3D TOF-MRA, axial MIP, rotated 90° counterclockwise to correspond with the ultrasound image. Note the fetal-type PCA (arrow). Its elongated course deﬁ nes its nature as a fetal-type variant, whereas the PCoA reveals a more rectangular appearance. (E,F) In contrast to the increased ﬂ ow velocity in the PCoA, the fe- tal-type PCA has a normal ﬂ ow velocity (55/16 cm/s).

Fig. A5.139 (A) 3D TOF-MRA, coronal MIP corresponding with a proximal BA occlusion (arrow). Note the missing mid part of the BA (arrows) and the visualization of the distal BA (arrowhead). (B) TCCS, transforaminal approach, color-mode and corresponding Doppler spectra at diﬀ erent depths from 74 to 89 mm. At 74 mm a high pulsatile signal is seen (62/13 cm/s). A progressive loss of velocity down to a systolic ﬂ ow of 9 cm/s and a diastolic zero ﬂ ow is observed when insonating step-by-step up to a depth of 87 mm— ﬁ ndings compatible with a proximal BA occlusion. (C) TCCS, transfo- raminal approach, color-mode and corresponding Doppler spectra. The color-mode image revealed a retrograde ﬂ ow signal assumed to be the distal BA. Doppler spectra analysis conﬁ rms a retrograde ﬂ ow of the BA at a depth of 91 mm.

<<< < Предыдущая 6 7 8 9 10 11 12 13 14 15 16 1718 / 5018 19 20 21 22 23 24 25 26 27 28 29 30 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
30.08.202663 Мб0Книга_5771_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_5772_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202657 Мб0Книга_5774_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202656 Мб0Книга_5775_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202653 Мб0Книга_5776_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202651 Мб0Книга_5777_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202648 Мб0Книга_5778_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202642 Мб0Книга_5779_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202678 Мб0Книга_578_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202642 Мб0Книга_5780_Библиотеки_им_академика_М_И_Перельмана.pdf