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459Discussion

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.

contrast-enhanced (ce) 3D MRA suﬀ ers from restricted spatial resolution as compared with DSA and CTA, due to the large ﬁ eld of view. MR perfusion, usually performed using T2* sequences, does not allow precise parametric quantiﬁ cation because signal loss and ﬂ ow impairment are not correlated in a linear manner. In contrast, CTA provides high-resolution vessel imaging in combination with quantitative perfusion measurement and has become the leading cross-sectional imaging modality in VS. In a recent meta-analysis, CT perfusion deﬁ cits represented a signiﬁ cant ﬁ nding in determining DID in aneurysmal SAH (Mir et al 2014). Because not all patients with focal neurologic deﬁ cits show angiographic VS and not all patients with VS show neurologic deﬁ cits, the concept of identi- fying patients at risk for DID requires more than vessel imaging. In a retrospective cohort of 96 patients, new CT perfusion deﬁ cits, identiﬁ ed by prolonged mean transit time (MTT) and reduced CBF, were signiﬁ cantly associat- ed with subsequent infarction and permanent neurologic deﬁ cits (Sanelli et al 2013). With the introduction of volume CT scanners, whole-brain CT perfusion analysis has become available, which is a promising approach for v i s u a l i z a t i o n o f f o c a l p e r f u s i o n d e ﬁ cits in VS patients (Dolatowski et al 2014).

Practical Recommendations for an Ultrasound Protocol

TCCS is the preferred method if available. In appropriate vessels (straight segment, at least 1 cm visible, sample volume positioned in or near the center of the visible vessel) angle-corrected ﬂ ow velocity measurements can be per- formed. Peak systolic ﬂ ow velocity measurement is rec- ommended instead of V distal), proximal M2-MCA, A1-ACA, P1- and P2-PCA (proximal and distal), and terminal ICA should be routinely studied as well as the V4-VA and BA. To identify hyperemia, the

. The M1-MCA (proximal and

mean

MCA/BVR velocity ratio can be added to the MCA/extracranial ICA velocity ratio. In vertebrobasilar aneurysm the BA/ extracranial VA velocity ratios should be included. Initial examinations should be performed as early as possible to establish the patient’s normal values. TCCS should then be repeated daily in the ﬁ rst week and followed daily until a plateau is reached. Depending on the clinical status the examination should then be performed every second day or in larger intervals for the following 2–3 weeks. If rapidly increasing ﬂ ow velocities are detected, ultrasound inter- vals should be adapted and may be performed twice daily.

If the LI is >3, a circumscribed peak systolic velocity of 150 cm/s is the preferred threshold for VS diagnosis in the M1-MCA (Krejza et al 2005). This value corresponds to the threshold recommended by Baumgartner and colleagues (1999) for MCA stenoses <50% (with a range of 22–48% and a mean of 36%). Still following the Baumgartner criteria, a peak systolic velocity ≥220 cm/s determines severe MCA VS with a lumen reduction ≥50%. In M2-MCA segments, 100 cm/s can be used as a cut-oﬀ value (mean peak systolic velocity of normal population plus two standard deviations) (Rogge et al 2015). For the A1-ACA and P1/P2-PCA segments, again the Baumgartner thresholds should be used with a peak systolic velocity ≥120 cm/s for the ACA and ≥100 cm/s for the PCA in mild to moderate VS (lumen reduction up to 50%) and ≥155 cm/s and ≥145 cm/s, respectively, for severe VS (lumen reduction ≥50%). For ICA assessment, threshold values of the ACA may be considered. For the BA, a circumscribed peak ﬂ ow velocity ≥100 cm/s and ≥140 cm/s can be assumed as mild to moderate VS and severe VS, respectively, if the SI is >2. Because of sometimes long segmental stenosis in VS and increased ICP, lower ﬂ ow velocities may be seen compared with a circumscribed atherothrombotic stenosis. In case of doubt, secondary signs (poststenotic ﬂ ow pattern in more distal vessel segments and/or collateral ﬂ ow in the unaﬀ ect- ed basal arteries) should be searched for, assuring severe vessel obstruction.

460

Case 34

Right-sided Occipital Dural Arteriovenous Fistula

Clinical Presentation

A 20-year-old woman was admitted with a right-sided parietooccipital headache. Three years earlier, she had a cerebral venous thrombosis (CVT) in the right transverse (TS) and sigmoid sinus (SiS). The CVT was likely the combined result of a heterozygote plasminogen activator inhibitor type 1 deﬁ ciency (PAI-1), a prothrombin mutation, and oral contraceptives. She was administered oral anticoagulation for 12 months. The current headaches seemed similar to those described 3 years before and she feared a relapse. She also reported a right- sided pulsatile tinnitus which started roughly 6–9 months after CVT. Despite its unremitting daily persistence, she had adapted to the noise. An outpatient otorhinolaryngology consultation revealed nothing remarkable and no accompanying symptoms were reported. Her neurologic status was within normal limits. The right occipital artery (OccA) was easily palpable and digital compression led to mild amelioration of her tinnitus. Clinically, we suspected that an occipital dural arteriovenous ﬁ stula (DAVF) had formed as a sequel to her CVT.

Initial Neuroradiologic Findings

Cerebral MRI showed no old or acute parenchymal lesions (not shown). Source data of the 3D time-of-ﬂ ight MR angiography (TOF-MRA) revealed irregular signal appearance in the right SiS which was assumed to present arterialized venous vessels. The distal SiS seemed occluded (Fig. B34.1) and the right OccA and middle meningeal arteries (MMA) were prominent (Fig. B34.2). Finally, 3D TOF-MRA showed arterialized right proximal SiS and TS as well as prominent right OccA and MMA (Fig. B34.3

and Fig. B34.4).

Suspected Diagnosis

Occipital right-sided DAVF fed by the right MMA and OccA based on a former CVT.

Questions to Answer by Ultrasound Techniques

• Could the feeding arteries be identiﬁ ed by ultrasound?

• Could the draining veins be identiﬁ ed?

• What was the shunt volume?

• Could the ﬁ stula state be estimated according to Cognard?

Initial Neurosonologic Findings

Extracranial Duplex Sonography

Because we suspected DAVF, blood volume ﬂ ow (BVF) measurements were performed in addition to the standard ﬂ ow velocity assessment. Comparison of the right and left sides revealed increased ﬂ ow velocity and BVF in the right common carotid artery (CCA) and right external carotid artery (ECA) compared with the left-side vessels. Pulsatility was accordingly reduced in the right CCA and ECA, and the right ECA had an increased diameter (5.4 versus 3.6 mm) (Figs. B34.5– B34.11). A marked hyperperfusion was also detected in the right-sided OccA, again with concomitantly reduced pulsatility index (PI) (Fig. B34.12 both internal carotid arteries (ICAs) and vertebral arteries (VAs) was normal.

The examination of the venous drainage revealed a mild left-sided ﬂ ow dominance via the internal jugular veins (IJVs) (Fig. B34.14 dominance was also observed in the vertebral veins (VVs) (Fig. B34.16 OccA led to a reduced ﬂ ow in the left IJV. Also, the previ- ous monophasic ﬂ ow changed to a biphasic ﬂ ow pattern (Fig. B34.18). Global cerebral circulation time measured between the left CCA and left IJV after echo contrast agent injection was ~2 seconds).

and Fig. B34.17). Compression of the right

Transcranial Duplex Sonography

Normal blood ﬂ ow parameters were seen in all basal cerebral arteries on both sides. The MMA was detectable on both sides and revealed an internalized ﬂ ow signal with increased ﬂ ow velocity and decreased pulsatility on the right side and a normal signal contralateral (Fig. B34.19 normal ﬂ ow signals in the basal vein of Rosenthal (BVR) on both sides as well as in the vein of Galen and straight sinus (StS) revealing peak systolic ﬂ ow velocities of ~10 cm/s. However, we observed a prominent antegrade ﬂ ow at the left TS. The main ﬁ nding was a marked ret- rograde ﬂ ow in the right TS with a peak systolic ﬂ ow velocity of 25 cm/s (Fig. B34.21

and Fig. B34.20). Venous analysis showed

and Fig. B34.13). Assessment of

and Fig. B34.15). A left-sided

and Fig. B34.22).

461Initial Neurosonologic Findings

Fig. B34.1 (A,B) Source images of a 3D ce-MRA, axial plane, showing signal irregularities of the right sigmoid sinus (arrows) considered to be partial recanalization or arterialization.

Fig. B34.2 (A) Raw-data TOF-MRA, axial plane, showing enlarged OccA on the right side (arrow). (B) Ce-MRA, axial plane, revealing a prominent middle meningeal artery (arrow). No corresponding artery is seen on the contralateral side.

Fig. B34.3 3D TOF-MRA, axial maximal intensity projection (MIP), suggestive of a DAVF, showing a prominent ﬂ ow signal in the right TS indicating arterialization (arrowhead) and marked signals of the assumed middle meningeal artery (arrow) and its branches (white arrows).

CCA-R BVF

Fig. B34.5 Extracranial duplex, longitudinal plane. Right CCA with increased BVF and reduced pulsatility in comparison to the contralateral side (BVF 500 mL/min, PI = 1.5).

Fig. B34.4 3D TOF-MRA, coronal MIP, suggestive of a DAVF, showing a prominent ﬂ ow signal in the right TS indicating arterialization (small arrowhead) and marked signals of the OccA (arrow) and branches of the middle meningeal artery (white arrows). The center of the DAVF is marked by the large arrowhead.

CCA-L BVF

Fig. B34.6 Extracranial duplex, longitudinal plane. Left CCA with normal BVF and pulsatility (BVF 380 mL/min, PI = 2.19).

462 Case 34 Right-sided Occipital Dural Arteriovenous Fistula

ICA-R BVF

Fig. B34.7 Extracranial duplex, longitudinal plane. Right ICA with normal BVF (210 mL/min).

ECA-R BVF

ICA-L BVF

Fig. B34.8 Extracranial duplex, longitudinal plane. Left ICA with normal BVF (250 mL/min).

ECA-L BVF

Fig. B34.9 Extracranial duplex, longitudinal plane. Right ECA with BVF increase and low PI in comparison to the contralateral side (BVF 350 mL/min, PI = 1.36).

ICA-R

ECA-R

ICA-R

Fig. B34.11 Extracranial duplex, color-mode image, axial plane. (A) Note that the diameter of the right ECA exceeds the diameter of the ICA. (B) Normal and physiologic relation of larger ICA and smaller ECA diameter on the left side.

Fig. B34.10 Extracranial duplex, longitudinal plane. Left ECA with normal BVF and pulsatility (BVF 130 mL/min, PI = 2.56).

OccA-R BVF

Fig. B34.12 Extracranial duplex, axial plane. Right OccA with increased BVF and decreased PI (BVF 210 mL/min, PI = 1.34).

463Initial Neurosonologic Findings

OccA-L BVF

Fig. B34.13 Extracranial duplex, axial plane. Left OccA with normal ultrasound parameters (BVF 20 mL/min, PI = 3.17).

IJV-L BVF

IJV-R BVF

Fig. B34.14 Extracranial duplex, longitudinal plane. Right IJV with normal BVF (430 mL/min).

VV-R BVF

Fig. B34.15 Extracranial duplex, longitudinal plane. Left IJV with normal BVF (490 mL/min).

VV-L BVF

Fig. B34.17 Extracranial duplex, longitudinal plane. Left VV with BVF in the normal range (40 mL/min).

Fig. B34.16 Extracranial duplex, longitudinal plane. Right VV with BVF in the normal range (10 mL/min).

IJV-L during compression of OccA-R

Fig. B34.18 Extracranial duplex, longitudinal plane. During compression of the right OccA (white dotted line) the ﬂ ow spectrum changes from monophasic to biphasic. Also, the diastolic ﬂ ow markedly decreases, which indicates reduced ﬁ stula ﬂ ow from the right OccA into the left IJV during compression.

464 Case 34 Right-sided Occipital Dural Arteriovenous Fistula

MMA-R

Fig. B34.19 TCCS (transtemporal approach), right-sided insonation, axial lower pontine plane. Right MMA with internalized ﬂ ow signal comprising high diastolic ﬂ ow (ﬂ ow velocity 48/19 cm/s, PI = 0.9).

TS-R

MMA-L

Fig. B34.20 TCC S (t rans tempo ral ap proa ch), l eft- sided inson ation, axial lower pontine plane. Left MMA with normal ﬂ ow signal and lower velocities compared with the right MMA (ﬂ ow velocity 26/5 cm/s, PI = 1.75).

TS-L

Fig. B34.21 TCCS (trans temp oral ap proa ch), left-s ided ins onati on, oblique midbrain plane. The right TS revealed a marked retrograde ﬂ ow signal with increased pulsatility (ﬂ ow velocity 25/16 cm/s).

Conclusion

Right-sided occipital DAVF as a long-term result of right TS and SiS thrombosis. Blood supply via branches of the right ECA (mainly the OccA and MMA) with predominant drainage into the left TS and IJV. A type IIa ﬁ stula accord- ing to Cognard (Cognard et al 1995) with a retrograde drainage into a main dural sinus was diagnosed.

Conventional Angiography

Digital subtraction angiography (DSA) was performed to exclude venous congestion and to consider therapeutic options. The suspected occipital DAVF with the right MMA and OccA as main feeders based on an occlusion of the right SiS with compensatory venous outﬂ ow via the

Fig. B34.22 TCCS (trans temp oral ap proa ch), left-s ided ins onati on, oblique midbrain plane. The left TS revealed a marked antegrade ﬂ ow signal (ﬂ ow velocity 20/14 cm/s).

contralateral TS toward the left TS and IJV were conﬁ rmed. In addition to the known feeders, DSA also detected tentorial branches of the right ICA and meningeal branches of both VA. No retrograde venous ﬂ ow into cerebral veins was detected and a grade IIa Cognard was aﬃ rmed (Fig. B34.23, Fig. B34.24, Fig. B34.25, Fig. B34.26).

Clinical Course (1)

The headache spontaneously remitted within 2 days and was considered unspeciﬁ c. At discharge 4 days later, the pulsatile tinnitus remained unchanged. Based on the low Cognard grade of IIa and the complex vascular architecture with feeders from a variety of vessel territories, we decided not to treat the ﬁ stula using interventional or surgical treatment.

465Discussion

Fig. B34.23 (A) DSA, right selective ECA injection, posteroanterior view, early arterial phase. Right-sided occipital DAVF with the OccA (large arrows) and the MMA (short arrows) as the main feeders. Note the early contrast ﬁ lling of the distally occluded SiS (arrowhead). (B) In the late arterial phase the arterial ﬁ stulas are hardly visible, while the ﬂ ow from the retrograde right TS into the left TS and IJV be- comes clearly visible (curved arrow). As no retrograde cortical venous ﬁ lling was detected, a grade IIa according to Cognard was diagnosed.

Fig. B34.25 DSA, selective right VA injection, posteroanterior view (A) and lateral view (B), early arterial phase. Prominent branches from the right V3-VA segment at the atlas arch directly drain into the right SiS resulting in a more complex DAVF architecture.

Clinical Course (2)

The patient was seen after 1 year for a ﬁ rst clinical fol- low-up. She reported unchanged complaints of a moderate right-sided pulsatile tinnitus. MRI was unremarkable and ultrasound ﬁ ndings appeared identical to the ﬁ rst examination.

Final Diagnosis

Right-sided occipital DAVF grade IIa according to Cognard following CV T of the right TS and SiS 3 years ago. The headache remitted spontaneously after 1 week while the pulsatile tinnitus remained during the follow-up period of 1 year.

Fig. B34.24 DSA, right selective ECA injection, lateral view, early arterial phase. Note the marked ﬂ ow into the right SiS via prominent branches of the MMA (arrows). The origin of the MMA at the foramen spinosum is visible (arrowhead). Note also the course of the STeA with its typical elongated course, not activated as a feeder (arrow).

Discussion

Clinical Aspects

Here, we describe a patient with transient parietooccipital headache and right-sided pulsatile tinnitus caused by a DAVF located at the junction of the TS and SiS. The diagnosis was already clinically suspected, as the patient had suﬀ ered from a CVT of the ipsilateral TS and SiS 3 years previously. Characteristic ﬁ ndings in MRI, MRA, and ul- trasound made the diagnosis very likely and it was ﬁ nally conﬁ rmed by DSA.

DAVFs consist of abnormal shunts between dural branches of extracranial arteries and dural venous sinus or cortical leptomeningeal veins and comprise around 10% of all intracranial arteriovenous malformations (Awa d et al 19 90) . Pr eci se epi dem iol ogi c data are mi ssing, however. A Japanese study reported an incidence of

0.29/100,000 adults per year. Age of the clinical manifestation is variable, with a peak in the ﬁ fth to seventh dec- ades of life (Cognard et al 1995).

The pathophysiology of DAVFs is still not completely understood. Generally, they are acquired malformations and occur spontaneously in association with trauma, iatrogenically, or secondary to aneurysmal rupture, or spontaneously (idiopathic), probably via the opening of previously involuted microarteriovenous communications rather than congenitally as in arteriovenous malformation (AVM). (For further reading, see Case 4, Case 32, and Case 40.) Probably the most important precondition for DAVF development is, however, an impaired intracranial venous outﬂ ow which can be caused by venous stenosis or more typically, CVT. The latter is present in around two-ﬁ fths of DAVFs, independent of anatomic location and gender (Tsai et al 2004a). CVT is also associated with a more

466 Case 34 Right-sided Occipital Dural Arteriovenous Fistula

Fig. B34.26 (A) DSA, right selective right ICA injection, lateral view, a further feeder was seen starting from a tentorial branch of the proximal carotid siphon (artery of Bernasconi) (arrow). (B) DSA, selective left VA injection, lateral view early arterial phase. Also the left VA showed a branch draining into the ﬁ stula (arrow).

severe clinical course (Tsai et al 2004b). Intracranial venous hypertension seems to trigger the opening of pre-existing arteriovenous communications with shunting between emissary arteries and veins or between vasa vasorum and small venous tributaries or dural sinuses. Furthermore, venous hypertension and CVT may induce a local inﬂ ammation with expression of several vascular growth factors resulting in angiogenesis (Uranishi et al 1999). For further reading on CVT, see Case 29.

The anatomic location of DAVFs is variable with typical areas of predilection. Up to 50% of all DAVFs are— as in our patient—located at the transverse–sigmoid junction (Hacein-Bey et al 2014, Santillan et al 2013). The main feeding arteries are normally transmastoid branches of the OccA and branches of the MMA (Tee et al 2013). Further typical feeders are meningeal branches of the VAs, the ascending pharyngeal artery, and tentorial branches of the ICA. Next to the occipital DAVFs, carotid-caver nous sinus ﬁ stulas (CCSF) are the second most common location. Typically in case of a severe head trauma, the ICA itself or branches of the ICA or ECA are the feeding arteries, often revealing a high shunt volume. CCSF is especially frequent in Asia which is likely, at least in part, attributable to facial acupuncture (Chung et al 2002, Hacein-Bey et al 2014). Less common DAVFs are fed by (1) meningeal arteries and drain into the superior sagittal sinus (SSS), and (2) tentorial and ethmoidal arteries which drain primarily into the deep cerebral venous system and frontal cortical veins (Chung et al 2002, Santillan et al 2013).

The clinical presentation of DAVFs is highly variable and depends on location, size, and drainage type of the ﬁ s- tula. Some DAVFs remain asymptomatic for decades and undergo spontaneous remission (Bitoh and Sakaki 1979, Hansen and Sogaard 1976, Luciani et al 2001, Magidson and Weinberg 1976, Olutola et al 1983). In many patients, symptoms are related to intracranial hemorrhage or to intracranial venous hypertension (e.g., seizures, headache, focal neurologic deﬁ cits, dementia, and parkinsonism).

In cavernous sinus aﬄ iction, orbital signs like exophthal- mos, conjunctival injection, and diplopia are the main clinical signs. Pulsatile tinnitus occurs in 20% of all DAVF patients but is observed in nearly 100% of occipital DAVFs located at the transverse–sigmoid junction because of its close anatomic relationship to the inner ear (Chung et al 2002, Kim et al 2002, Santillan et al 2013). However, pulsatile tinnitus is not pathognomonic for DAVFs. In a large series of 84 patients, a DAVF was diagnosed in 27% (23 patients, 6 CCSF, and 17 non-CCSF). ICA stenosis due to atherosclerosis, dissection, or ﬁ bromuscular dyspla- sia was found in 20%. CVT, glomus tumors, intracranial hypertension, or other reasons accounted for 20% while the cause remained unclear in 32% of patients (Waldvogel et al 1998).

A simple clinical test is extremely helpful for initial

diﬀ erentiation: namely, if compression of the ipsilater- al OccA reduces or stops pulsatile tinnitus, it is highly likely that there is an underlying occipital DAVF fed by the OccA. Conversely, compression that does not result in decreased tinnitus is a strong indicator that no occipital DAVF is present.

The risk of intracranial hemorrhage and severity of clinical symptoms is mainly deﬁ ned by the venous drain- age pattern. DAVFs with a retrograde drainage into cortical leptomeningeal veins show a much higher risk of having an aggressive clinical course that requires prompt interventional treatment. Two patterns can be separated. The ﬁ rst leads to brain edema caused by venous conges- tion and venous hypertension. The second consists of intracranial hemorrhage caused by rupture of the distended leptomeningeal veins (Liu et al 2009).

All DAVF grading systems refer to the type of venous drainage. The classiﬁ cation according to Cognard and coworkers deﬁ nes ﬁ ve grades. In grade I, the ﬁ s- tula merges into an ipsilateral dural sinus with antegrade ﬂ ow. In grade II, there is either retrograde ﬂ ow into the dural sinus(es) (IIa), via a sinus into cortical vein(s) only (IIb), or into sinus(es) and cortical vein(s) (IIa + b). A ﬁ stula running directly into cortical veins without venous ectasia deﬁ nes grade III and one with venous ectasia (>5 mm and three times larger than the diameter of the draining vein) grade IV. In grade V, the intracranial ﬁ stula drains into the spinal medullary veins (Cognard et al 1995). Cognard type I is most commonly observed. In a large case series including 102 patients, type I was reported in 39% of patients, followed by type IIa (14.5%), type III (12.5%), type IV (12%), type IIa + b (10%), type IIb (8%), and type V (4%) (Davies et al 1996). DAFVs may also be graded into only three types, which can be matched with the Cognard criteria (Borden et al 1995). However, the Cognard classiﬁ ca- tion is of greater prognostic value and is therefore most frequently used (Davies et al 1997).

Cognard I and IIa can be considered benign variants as there is no increased risk of cerebral venous hypertension, bleeding, or dementia. The risk of hemorrhage or death is therefore practically 0%. DAVFs may change their characteristics over time and may even show spontaneous occlusion, particularly in low grade DAVFs (I–IIa). The remaining types (Cognard IIb–V) potentially lead to increased venous hypertension with increased morbidity

467Discussion

and an annual mortality of up to 10% (Cognard et al 1995, Satomi et al 2002, van Dijk et al 2002). In patients with venous ectasia (Cognard IV) the annual morbidity may be as high as 27% (Bulters et al 2012). Early rebleeding risk after a ﬁ rst hemorrhage in patients with cortical reﬂ ux was reported to be 35% within the ﬁ rst 2 weeks (Duﬀ au et al 1999). Interventional therapy is therefore recommended in higher grade DAVF (IIb–V) with cortical venous reﬂ ux. However, even in ﬁ stulas with cortical venous re- ﬂ ux, spontaneous occlusion can be observed (van Dijk et al 2002).

A separate classiﬁ cation has been recommended for CCSF. Here, type A indicates a direct connection between the intracavernous segment of the ICA and the cavernous sinus (CS) seen after trauma. Type B–D refers to indirect connections of the CS via branches of the ICA (type B), the ECA (type C), or both (type D; Barrow et al 1985).

Treatmen t option s, if i ndicated, are endovasc ular, open surgery, and radiotherapy, or a combination of these methods. Currently, endovascular embolization is considered to be the method of choice, especially in DAVFs with multiple arterial feeders (Urtasun et al

1996). A transvenous approach is preferred if the entire venous drainage pathway of the DAVF is accessible by retrograde catheterization. Occlusion of the venous collectors can be performed by coils if necessary in combination with embolic materials. Transarterial access is reserved for patients with impaired venous access, e.g., in cases with stenosis, occlusion, or compartmentalization of the venous drainage system. Surgery should be considered if endovascular treatment alone is unsuccessful (Kakarla et al 2007). Transarterial embolization may be used before surgery to reduce the amount of blood ﬂ ow (Liu et al 2009). The need for surgical treatment essentially depends on the anatomic location of the ﬁ stula and is mainly recommended in DAVFs with venous congestion and cortical venous drainage of the anterior cranial fossa, the tentorium, or the SSS and in cases with intracerebral hemorrhages (Davies et al 1997, Miller and Gandhi 2015). Radiosurgery can be considered as another second-line treatment option with obliteration rates between 50% and 75% (Miller and Gandhi 2015). The obliteration process usually takes several years, however, which leaves radiotherapy unsuitable for treatment of aggressive DAFVs with a high risk of hemorrhage (Liu et al 2009).

For our patient, the therapeutic options were interdisciplinary and warranted neurology, neurosurgery, and neuroradiology consultation. Due to the nonaggressive Cognard type IIa and the very low risk of intracranial hemorrhage or venous infarction and spontaneous remission of complaints, no invasive therapy was recommended. The headaches regressed and the clinical course over 1 year remained unchanged without new clinical symptoms.

A further empirical method to treat DAVFs is manual compression therapy. Repetitive compression of the ECA or OccA may induce thrombosis, especially in small DAVFs of the CS, TS, or SiS. The eﬃ cacy of this method is contro- versial, although success rates of up to 30% are reported (Halbach et al 1987a, 1987b, Higashida et al 1986, Schumacher and Szczeponik 2007). However, the potential

beneﬁ t is delayed. Schumacher, for example, described a successful treatment 19 months after the initiation of the treatment with more than 13,000 individual manual compression maneuvers (Schumacher and Szczeponik

2007). In our experience, at least in the most common occipital type I DAVF, manual compression therapy of the OccA can be recommended for the relief of tinnitus.

Angiologic and Anatomic Aspects

TCCS may allow direct color imaging of the DAVF itself depending on its size and location (Duan et al 2008). In particular, DAVFs with drainage into the CS or SiS/TS junction and with multiple feeding arteries are more likely to be detected than DAVFs draining into the SSS or cortical veins or those with a single feeder. Color duplex then demonstrates the ﬁ stula as a mosaic color pattern with a clear boundary corresponding to multidirectional turbulent blood ﬂ ow (Duan et al 2008).

The domain of extra- and transcranial ultrasonography, however, is the assessment of the arterial feeder and the venous drainage. Starting with the arterial vessels, the high shunt ﬂ ow can be detected by increased ﬂ ow veloc- ities, increased BVF, and decreased pulsatility or resistance. In extremely high ﬂ ow ﬁ stulas these criteria may be seen in proximally located arteries, as is the case in the most common type I occipital DAVF, e.g., in the CCA or ECA. In occipital ﬁ stulas with lower shunt volume, the ﬂ ow parameter changes only become evident in more distally located arteries, e.g., the OccA itself. The probability of detecting a ﬁ stula therefore depends on shunt magnitude and location.

The OccA can be detected in 100% of healthy subjects, even with its usual low ﬂ ow, by duplex sonogra- phy (Tee et al 2013) (for ultrasound identiﬁ cation, see also Chapter 2, “Occipital Artery” under “Special Arterial Anatomy and Ultrasound Anatomy”). If it is recruited as a feeder, a pathologic OccA ﬂ ow pattern is detectable in almost all patients. Bilateral examination and meticulous comparison of both ﬂ ow signals is mandato- ry in pulsatile tinnitus in order not to overlook a low ﬂ ow ﬁ stula (Arning et al 2005, Duan et al 2008, Tee et al 2013). In a large study including 181 patients with DAVFs at diﬀ erent sites, a resistance index (RI) <0.76 in the OccA yielded a sensitivity, speciﬁ city, PPV, and NPV of 96%, 97%, 92%, and 98%, for the detection of the DAVF. Corresponding values for end- diastolic ﬂ ow ve- locities >14 cm/s were 96%, 95%, 88%, and 98% (Tee et al

2013). Blood ﬂ ow alterations in the ECA are similar to those in the OccA, although the diagnostic accuracy is slightly lower in patients with a feeding OccA. For a RI <0.72 in the ECA, sensitivity, speciﬁ city, PPV, and NPV of 74% 89%, 79%, and 86% have been reported. Corresponding values for end-diastolic ﬂ ow velocities using a cut-oﬀ >24 cm/s were less useful: 60%, 83%, 66%, and 79% (Tsai et al 2004b). Postinterventional increase of the RI in the ECA then indicates successful treatment of DAVF (L.K. Tsai et al 2005). A low resistance or low pulsatility of the ECA, however, is not speciﬁ c for a DAVF and may also be observed as a sign of orbital collateral ﬂ ow in hemodynamically relevant high-grade ICA

468 Case 34 Right-sided Occipital Dural Arteriovenous Fistula

stenosis or occlusion. Parameters with lower DAVF detection sensitivities are the ICA/ECA and the bilateral ECA ratio of RI (Tsai et al 2009). As shown in our case, MMA examination by TCCS may yield valuable information, although this approach is not yet part of a routine diagnostic ultrasound protocol in suspected DAVF (for further reading on MM A, see Chapter 2, “Excursion: Middle Meningeal Artery” under “Special Arterial Anatomy and Ultrasound Anatomy”).

Volume ﬂ ow measurements may also be indicative of DAVFs and CCSF. Analysis of 14 CCSF patients yielded increased ICA ﬂ ow in almost all type A cases but was normal in types B–D. Increased ECA BVF was found in types C and D (Lin et al 1994). In a combined study of 30 patients with CCSFs or DAVFs, the best results were achieved using an ECA ﬂ ow cut-oﬀ >260 mL/min which yielded a sensitivity, speciﬁ city, PPV, and NPV of 51%, 89%, 72%, and 77%. The low sensitivity can probably be attributed to the inclusion of patients with CCSF (Tsai et al 2004b).

The analysis of potential venous drainage vessels in assumed DAVFs and patients with pulsatile tinnitus is even more neglected than the assessment of the arterial part of the circulation. TCCS allows the analysis of intracranial draining veins and sinuses in DAVF. Characteristically, the BVF of the involved veins and sinuses is markedly increased (Chiou et al 1998, Duan et al 2008, Harrer et al 2005). In CCSF, the examination of the superior ophthalmic vein shows a retrograde ﬂ ow with increased ﬂ ow velocity and reduced pulsatility which normalizes after ﬁ stula occlusion (Chiou et al 1998). Harrer and coworkers compared contrast-enhanced TCCS with DSA in 20 patients with occipital DAVFs and found 93% of draining veins and sinuses deﬁ ned by peak systolic ﬂ ow velocities >50 cm/s. More speciﬁ cally, the drain- ing TS (9 of 9), superior petrosal sinus (5 of 5), SiS (4 of 4), BVR (3 of 3), and StS (3 of 3) were correctly detected in all cases. The SSS venous drainage pathway was, however, correctly recognized in only one of three cases. After transcatheter embolization, the mean reduction of blood ﬂ ow velocity was 44 ± 18% compared with pretreatment values (Harrer et al 2005). Therefore, drainage into the SSS and cortical veins can hardly be observed by TCCS because of the deep and obscured location (Duan et al 2008, Harrer et al 2005).

Systematic duplex sonography analyses of the cervical venous drainage pattern in patients with DAVF are missing. Signs of hyperperfusion—deﬁ ned as an increased BVF and raised ﬂ ow velocities—as well as “arterialized” ﬂ ow signals in the IJV or VV should be evaluated. Our patient, with a right-sided DAVF type IIa, showed a dominant drainage via the left IJV with almost normal ﬂ ow appearance

The global cerebral circulation time (gCCT) is a newer diagnostic tool to assess DAVF using Doppler or duplex sonography. The gCCT, deﬁ ned as the time in- terval of contrast medium arrival between the ICA and the IJV (in healthy individuals about 6–7 seconds), is in most cases greatly shortened in patients with DAVF. In a group of 13 patients a mean gCCT of 1.1 ± 0.9 seconds (range: 0.4 – 2.6 seconds) was observed with a sensitivity, speciﬁ city, PPV, and NPV of 100%, 97%, 93%, and

100% compared with DSA for DAVF detection (Schreiber et al 2004). In our patient, a gCCT of about 2 seconds was seen, which corresponds well to the known reference data. Postinterventional normalization of gCCT with good correlation to treatment results suggests that the method might be suitable for therapy monitoring (Schreiber et al 2004). The individual gCCT depends on the DAVF type, however. In the DAVFs with direct shunting into a dural sinus, the gCCT is shorter than in DAVFs with drainage into cortical veins. In the latter case, the gCCT can also be normal (personal observation). Here, intracranial veins can be observed in unusual sites with increased ﬂ ow velocities and also ﬂ ow turbulences, given a suspicion of an abnormal intracranial venous circulation of unknown origin. The DAVF drainage type should also be considered when choosing the optimal side of gCCT measurement as type I drains toward the ipsilateral IJV but type IIa toward the contralateral IJV. When in doubt, patients with suspected DAVF and normal ipsilateral gCCT should additionally undergo measurements on the contralateral side to avoid false-negative results (see also Chapter 3, “Cerebral Circulation Time” under “Parameters of Cerebral Hemodynamics”).

There is no report of a systematic multiparametric DAVF ultrasound evaluation. Our recommendation is to perform an extended extra- and intracranial arterial and venous duplex ultrasound examination in all patients with suspected DAVF, i.e., in those with pulsatile tinnitus, oculopathy, or atypical brain edema with or without bleeding. When in doubt, the gCCT can be measured with echo contrast agents. In pulsatile tinnitus, the focus is more directed on the arterial side of the OccA. If possible, the MMA should also be studied. In suspected CCSF, the superﬁ cial temporal artery (STeA) and also transorbital- ly the orbital arteries and veins, especially the superior ophthalmic vein, should be insonated. Auscultation and vessel palpation may be of help and the eﬀ ect of compres- sion of the OccA and/or STeA on the tinnitus or oculopathy should be recorded.

CT and MRI are primarily used in patients with suspected DAVF (Gandhi et al 2012). Intraparenchymal, i n t r a v e n t r i c u l a r , o r s u b a r a c h n o i d h e m o r r h a g e a s w e l l a s associated hydrocephalus can conﬁ dently be diagnosed with these techniques. White matter hyperintensities in T2- or FLAIR MRI can be indicative for intracranial venous hypertension. ADC and diﬀ usion-weighted imaging can be pathologic in cases of cortical venous drainage with venous hypertension or ischemia (Sato et al 2011). Furthermore, venous thrombosis, dilated arterioles alongside the wall of dural sinuses, and venous ectasia can be observed by MRI and contrast-enhanced CT (Willinsky et al 1994, 1999). Conventional CT and MRI with MRA were shown to detect DAVFs in up to 70% (CT) and 81% (MRI), particularly by detecting dilated and elongated feeders from the ECA (Chung et al 2002). R e c e n t l y , a s e n s i t i v i t y a n d s p e c i ﬁ city of MRI compara- ble to DSA has been reported for DAVF assessment when investigating patients with pulsatile tinnitus (Deuschl et al 2015). Similar to AVM analysis, DAVF ﬂ ow dynamics can also be assessed in detail by modern time- resolved CTA (Brouwer et al 2010, Willems et al 2011) and

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