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419Discussion

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.

the SA pathology as well as its hemodynamic eﬀ ects. In particular, the late arterial phase images allow detection of the retrograde VA ﬂ ow if contrast is injected into the unaﬀ ected VA. In addition, DSA allows the assessment of other more complex vascular constellations, including the less frequently observed carotid-basilar, externo-vertebral, and carotid-subclavian collateral pathways. Like ultrasound techniques, DSA also allows functional or compression tests to be performed. Its main diagnostic pitfall is the aortic arch injection, which permits easy visualization of the SA pathology but may result in missing ipsilateral VA contrast ﬁ lling, suggesting VA occlusion. Also on selective contrast ﬁ lling of the unaﬀ ected VA, an evaluation limited to the early arterial phase might overlook a contralateral steal phenomenon. Because of the low morbidity of the SSP, DSA should no longer be used as the ﬁ rst method of choice.

TOF-MRA, as a ﬂ ow-sensitive technique, is not well suited to analysis of the SSP, as alternating ﬂ ow patterns will result in an absent vessel signal, suggesting VA occlusion. Contrast-enhanced (ce) MRA might suﬀ er the same problem in grade 2 SSP, but only if a net zero ﬂ ow (iden- tical systolic retrograde and diastolic anterograde ﬂ ow) is present. As this type of ideal alternating ﬂ ow is probably rare and a preponderance of either systolic or diastolic ﬂ ow occurs in the majority of cases, ce-MRA will be able to evaluate the vessel integrity. However, conﬁ rmatory

statements regarding the ﬂ ow direction within a vessel cannot be made with either method. Phase-contrast MRA can provide information on ﬂ ow direction, but preselec- tion of ﬂ ow velocity parameters is required and the tech- nique is therefore rather susceptible to misinterpretation (Drutman et al 1994). A dynamic MRI approach analyzing bolus kinetics after gadolinium injection may allow a more adequate assessment by analyzing the circulation time of a gadolinium bolus. In a small study including eight patients with SSP a delay of peak enhancement was observed in the aﬀ ected VA, ranging from 2 to 4 seconds, whereas none of the controls demonstrated a delay (Wu et al 2005). In another small case series, retrograde VA and/or delayed VA c on tr ast o n t he s id e a ﬀ ected by SSP was detected by using dynamic ce-MRA (Schubert 2010). When using CTA, appropriate contrast administration technique and postprocessing methods need to be used because of the inability of this technique to diﬀ erentiate ﬂ ow direction and its lack of hemodynamic time sequences. Otherwise there may be false-negative results, as has been shown in a case report (Ratanakorn et al 2002). Larger series of CTA use for SSP analysis have not been reported. The role of volume CT using multiple detector rows (i.e., 256–320) or ﬂ at-panel detectors remains to be determined, although the feasibility of ﬂ at-panel volume CT for SSP imaging has been demonstrated in experimental studies (Gupta et al 2011).

420

Case 29

Cerebral Venous Thrombosis

Clinical Presentation

A 34-year-old woman presented with a 2-day history of headache of ﬂ uctuating intensity. On the day of admission, the headache had worsened markedly and she had developed nausea and vomiting. No vascular risk factors were known except for smoking and a prescribed estrogen-containing contraceptive. On admission, the neurologic examination revealed no focal neurologic deﬁ cits or meningeal signs.

Initial Neuroradiologic Findings

Cranial CT did not demonstrate presence of ischemic p a r e n c h y m a l l e s i o n s . H o w e v e r , t h e r i g h t t r a n s v e r s e s i n u s (TS) appeared hyperdense (Fig. B29.1).

Suspected Diagnosis

Cerebral venous thrombosis (CVT) of the right TS.

Questions to Answer by Ultrasound Techniques

• Was the pulsatility index in the brain-supplying arteries raised as an indirect sign of increased intracranial pressure?

• Were there signs of intracranial venous collateral drainage pathways?

Initial Neurosonologic Findings (Day 1)

25/20 cm/s). No ﬂ ow signal could be detected in pro- jection of the right TS. The contralateral TS revealed raised ﬂ ow velocities (ﬂ ow velocity: 41/34 cm/s) (Figs. B29.2, Fig. B29.3, Fig. B29.4, Fig. B29.5, Fig. B29.6; see also Video

B29.1).

Conclusion

The neurosonologic ﬁ ndings were suggestive of a right TS occlusion because of the raised left TS ﬂ ow and of an additional superior sagittal sinus (SSS) ﬂ ow obstruction because of the raised ﬂ ow in the deep cerebral veins. The left TS and SpPS as well as both BVRs appeared as the main alternative drainage pathways.

CT Angiography (CTA) (Day 1)

CTA conﬁ rmed a thrombosis of the distal SSS extending to the right TS and sigmoid sinuses (SiS) down to the right superior jugular bulb (Fig. B29.7 and Fig. B29.8).

Clinical Course (1)

Intravenous heparin was initiated, aiming for a twofold increase of partial thromboplastin time (PTT). In the following 2 days the patient’s headache completely resolved. Treatment was then changed from heparin to oral anticoagulation with phenprocoumon. The etiology of the thrombosis remained unclear. There was no thrombophilia or underlying inﬂ ammatory dis- ease. Follow-up investigations were performed 90 and 180 days later.

Extracranial Duplex Sonography

B-mode sonography demonstrated normal ﬁ ndings in the carotid and vertebral arteries.

Transcranial Duplex Sonography

All intracranial arteries showed normal ﬂ ow signals with a regular pulsatility index of ~0.8, arguing against a severely raised intracranial pressure. Assessment of the intracranial veins revealed a prominent ﬂ ow signal in both basal veins of Rosenthal (BVRs) (ﬂ ow veloci- ty: left, 20/16 cm/s; right, 31/25 cm/s), the right deep middle cerebral vein (DMCV) (ﬂ ow velocity 29/25 cm/s), and the left sphenoparietal sinus (SpPS) (ﬂ ow velocity

Question to Answer by Ultrasound Techniques

• Was there evidence for recanalization of the occluded sinuses over time?

Follow-up Neurosonologic Findings (Day 90)

Transcranial Duplex Sonography

The BVR now revealed an almost normal but not completely normalized ﬂ ow signal on both sides (ﬂ ow velocity: left,

421Final Diagnosis

19/15 cm/s; right, 19/14 cm/s) (Fig. B29.9 and Fig. B29.10). Low ﬂ ow signals were also seen in the right DMCV and in the left SpPS (not shown). The TSs were not examined.

Conclusion

Marked improvement of the neurosonologic ﬁ ndings with diminished ﬂ ow velocity in the venous collateral vessels in- dicative of advanced recanalization of the right TS and SSS.

Question to Answer by Ultrasound Techniques

• Was there further evidence for normalization of venous hemodynamics?

Follow-up Neurosonologic Findings (Day 180)

Transcranial Duplex Sonography

Both BVRs now showed a completely normal ﬂ ow signal (ﬂ ow velocity: left, 11/9 cm/s; right, 14/11 cm/s). No ﬂ ow signals could be detected within the right DMCV and the

left SpPS. Both TSs revealed normal ﬂ ow signals (ﬂ ow ve- locity: left, 16/12 cm/s; right, 14/11 cm/s) (Fig. B29.11,

Fig. B29.12, Fig. B29.13, Fig. B29.14).

Conclusion

Complete normalization of intracranial venous h e m o d y n a m i c s i n d i c a t i v e o f v e s s e l r e s t i t u t i o n o f t h e r i g h t TS and SSS.

Clinical Course (2)

Clinical follow-up after 6 months was unremarkable. MRI after 6 months revealed no parenchymal lesions. Time-of-ﬂ ight MR angiography (TOF-MRA) demonstrat- ed a complete recanalization of the right TS and the SSS (Fig. B29.15). Anticoagulation with phenprocoumon was

Final Diagnosis

Extended CVT involving the distal SSS and the right TS, SiS, and jugular bulb. There was complete recanalization after 6 months while the patient was on oral anticoagulation.

Fig. B29.1 Unenhanced cranial CT, axial plane. No ischemic parenchymal lesions. Note the hyperdense right TS (arrows).

BVR-L

Fig. B29.2 TCCS (tr anst emporal appro ach) , left -sided insonati on, midbrain/thalamic plane. Mildly increased ﬂ ow in the left basal vein of Rosenthal (ﬂ ow velocity 20/16 cm/s).

422 Case 29 Cerebral Venous Thrombosis

BVR-R

Fig. B29.3 TCCS (transt empo ral ap proa ch), r ight -sided i nson ation , midbrain/thalamic plane. Increased ﬂ ow velocity in the right basal vein of Rosenthal (ﬂ ow velocity 31/25 cm/s).

SPhS-L

DMCV-R

Fig. B29.4 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Raised ﬂ ow velocity in the right DMCV (ﬂ ow velocity 29/25 cm/s).

TS-L

Fig. B29.5 TCCS (tr anst emporal appro ach) , left -sided insonati on, upper pontine plane. Flow velocity of 26/20 cm/s in the left SpPS.

Fig. B29.7 Intracranial CTA, sagittal maximal intensity projection (MIP). Lack of contrast enhancement within the posterior part of the SSS (arrows).

Fig. B29.6 TCCS ( tran stem pora l app roac h), right-sided insonation, oblique plane. Raised ﬂ ow velocities in the left TS (ﬂ ow velocity 41/34 cm/s).

Fig. B29.8 Intracranial CTA, coronal MIP. Thrombus extension into the right superior jugular bulb, as indicated by a lack of contrast ﬁ lling (arrow).

Final Diagnosis

423

BVR-L

Fig. B29.9 TCCS (tr anst empo ral app roac h), lef t-si ded in sonatio n, midbrain plane. Left basal vein of Rosenthal demonstrating an a l m o s t u n c h a n g e d ﬂ ow signal (ﬂ ow velocity 19/15 cm/s).

BVR-L

BVR-R

Fig. B29.10 TCCS (transtemporal approach), right-sided insonation, thalamic plane. Right basal vein of Rosenthal demonstrating a nearly normalized ﬂ ow signal (ﬂ ow velocity 19/14 cm/s).

BVR-R

Fig. B29.11 TCCS (t rans temp oral app roac h), lef t-s ided ins onat ion, midbrain plane. The left basal vein of Rosenthal in its proximal part showing a normal ﬂ ow signal (ﬂ ow velocity 11/9 cm/s). Note the cor- responding signal of the proximal P2-PCA (ﬂ ow velocity: 63/30 cm/s).

TSL-L

Fig. B29.13 TCC S ( tran stem pora l a ppr oach ), right-sided insonation, oblique plane. The left TS now reveals a normal ﬂ ow signal (ﬂ ow velocity 16/12 cm/s).

Fig. B29.12 TC CS ( tran stem pora l ap proa ch), r ight- side d in sona tion, thalamic plane. Normalized ﬂ ow signal in the right basal vein of Rosenthal (ﬂ ow velocity 14/11 cm/s).

TS-R

Fig. B29.14 TCCS (t rans temp oral ap proach) , left-sided insonation, oblique plane. The right TS can be visualized for the ﬁ rst time. There is a normal ﬂ ow signal (ﬂ ow velocity 14/11 cm/s).

424 Case 29 Cerebral Venous Thrombosis

Discussion

Clinical Aspects

Compared with arterial stroke, CVT is a rare condition. A hospital-based Dutch study in adults revealed an incidence of 1.32 per 100,000 population (Coutinho et al

2012). Important information regarding to clinical presentation, risk factors, and clinical course can be drawn from a large prospective multicenter study, the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), which was published in 2004 (Ferro et al 2004). The study included 624 patients aged 16–86 years (mean age 39 years), recruited in 89 centers in 21 countries. There was a female predominance (74.5% of cases) and headache was the principal symptom in 88.8%. In addition to the ISCVT data it should be mentioned that headaches in CVT either evolve within hours or may sometime even occur in the form of a thunderclap headache (de Bruijn et al 1996). Also, rarely CVT may present as SAH (Oppenheim et al 2005).

The main clinical signs in the ISCVT study were motor symptoms (37.2%) followed by papilledema (28.3%), mental disorders (22%), and aphasia (19.1%). Stupor or coma was present in 13.9% of patients. Seizures—usually focal with secondary generalization—occurred in 39.3% of cases. On MRI or CT, venous infarction was seen in 46.5%. Intracranial bleeding was found in 39.3%. Only 37.1% of patients were without detectable parenchymal pathology.

The most frequently aﬀ ected vessel in the ISCVT study was the SSS (62% of cases) followed by the lateral sinuses (TS and SiS), in 44.7% on the left side, and in 41.2% of cases on the right. The deep cerebral venous system was aﬄ ict- ed in 10.9% and the cortical veins in 17.1%. Only rarely was a thrombus of the cavernous sinus (CS) observed (1.3%). A combination of aﬀ ected sinus and veins is more the rule than an exception.

Depending on the aﬀ ected venous vessel, diﬀ erent clinical patterns can be distinguished. In isolated cortical vein thrombosis but also in cortical vein thrombosis with sinus thrombosis, focal deﬁ cits (motor, sensory, aphasia, neglect), headache, and epileptic seizures may occur. In isolated distal sinus thrombosis of the SSS and/or TS, no parenchymal lesion may be found. The clinical picture then resembles intracranial hypertension syndrome with diﬀ use headache, papilledema, and VIth nerve pal- sy. Thrombosis of the deep veins leads to often bilateral venous congestive lesions in the basal ganglia and thalami which results in an impaired consciousness and extrapyramidal signs. Finally, the rarely seen CS thrombosis mainly presents ocular signs with protruding eyes, papilledema, and IIIrd to VIth nerve palsies.

Thrombophilia in the ISCVT study was found in 34.1% and was inherited in most cases. This might be caused by antithrombin deﬁ ciency, protein C or S deﬁ ciency, factor V Leiden mutation, G20210A prothrombin gene mutation, or the controversial hyperhomocysteinemia due to gene mutations in methylene tetrahydrofolate reductase (MTHFR). An antiphospholipid antibody syndrome seen in 5.9% of cases was the main acquired disease in the ISCVT study. Other probable relevant causes were hematologic disorders such as general anemia occurring in 12%, and malignancy-related disorders in 7.4%. In females <50

Fig. B29.15 Intracranial 2D TOF-MRA, coronal MIP. Vessel normalization in the SSS and right TS after 6 months. Note the variation in the conﬂ uence of sinuses, with the SSS predominantly draining into the left TS, and the straight sinus predominantly draining into the right TS.

years of age, pregnancy and the puerperium were the presumed cause in 6.3% and 13.8%, respectively. Within this subgroup, oral contraceptives were taken by 54.3% of patients. In 12.5% of cases no risk factor could be identiﬁ ed. Iatrogenic CVT after lumbar puncture and subse- quent intracranial hypotension has to be mentioned as a rare cause of CVT. The postulated mechanism is a slowing of venous ﬂ ow which then facilitates thrombus formation (Yoon et al 2011). A study by Canhão and coworkers using TCD assessment of the straight sinus before, during, and after lumbar puncture conﬁ rmed this hypothesis, reveal- ing a sustained venous blood ﬂ ow velocity decrease after lumbar puncture (Canhão et al 2005). Finally, septic CVT may occur and has to be considered especially in children in the course of infections of the inner ear or mastoid (Acosta et al 2014) which may lead to a TS and/or SiS aﬀ ection.

CVT diagnosis is usually conﬁ rmed by neuroimaging (see below). In uncertain cases an elevated level of plasma D-dimer supports the diagnosis, but normal ﬁ ndings do not rule out CVT. It seems that the size of thrombotic material (large) and the stage of thrombus organization (fresh) increase the sensitivity and speciﬁ city of D-dimer testing. A large meta-analysis including 14 studies and 1,134 patients reported a sensitivity and speciﬁ city of 94% and 90% in patients with suspected CVT and of 89% and 83% in patients with conﬁ rmed CVT, respective- ly (Dentali et al 2012). In a recent study of 233 patients with suspected CVT and symptoms within the last 7 days, D-dimer had a sensitivity of 94% and speciﬁ city of 98% for accurate prediction of a CVT (Meng et al 2014).

The clinical outcome in the ISCVT study was favorable at a median of 16 months; 57.1% of patients were completely free of symptoms. Considering the modiﬁ ed Rankin Scale (m-RS), minor (m-RS: 1), mild

425Discussion

(m-RS: 2), moderate (m-RS: 3) and severe impairment (m-RS: 4 or 5) was seen in 22%, 7.5%, 2.9%, and 2.2%, respectively. Death occurred in 8.3% of cases. Recurrence was a minor concern aﬀ ecting only 2.2% of patients, but even second recurrences have been reported (Amberger et al 2006). Late epilepsy in the ISCVT study was seen in

10.6%. An unfavorable outcome was associated with central nervous system (CNS) infection, cerebral deep venous thrombosis, malignancy, age >37 years, psychiatric disorder, coma, intracranial bleeding, and male sex.

The majority of patients initially received anticoagulants (83.3%). Intravenous heparin was the mainly method used (64%). Low molecular weight heparin (LMWH) was given to 34.9%. A trend toward a better outcome concerning death and dependency was seen in patients who were anticoagulated (12.7%) compared with those who did not receive anticoagulation (18.3%). This diﬀ er- ence was, however, not statistically signiﬁ cant (Ferro et al 2004).

The main goal in the acute phase is to prevent propagation of the thrombus and to treat the generalized prothrombotic state. Anticoagulation with unfractionated heparin or LMWH is advocated by almost all centers since the publication of two randomized studies in 1991 and

1999. This is common clinical practice, despite the fact that these studies, and also a later meta-analysis, only showed a nonsigniﬁ cant reduction in the relative risk of death or dependency with anticoagulants (de Bruijn and Stam 1999, Einhäupl et al 1991, Stam et al 2002). LMWH seemed more favorable than unfractionated heparin. Nevertheless, the ISCVT study demonstrated that in clinical practice most patients do receive anticoagulation even in the presence of intracranial hemorrhages. In severe thrombotic processes and patients with progressive worsening, recanalization can be attempted. This can be performed by endovascular thrombolysis during which rt-PA or urokinase is injected into the aﬀ ected vessel or by mechanical thrombectomy with or without intrasinus thrombolysis (Siddiqui et al 2015). Currently, no controlled trials are available to prove their therapeutic effectiveness and the doses of thrombolytics administered vary widely.

In summary, and following the recommendation of the European Federation of Neurological Societies (EFNS), initial anticoagulation with dose-adjusted subcutaneous LMWH or intravenous heparin is recommended even in the presence of hemorrhagic venous infarction. LMWH is more eﬀ ective than unfractionated heparin and should be preferred unless interventions (lumbar puncture or surgery) are planned. In the case of clinical worsening despite adequate anticoagulation, endovascular thrombolysis should be considered. In large space-occupying brain lesions, unilateral or bilateral hemicraniectomy can be performed to prevent herniation if standard treatment protocols (controlled osmodiuretics, hyperventilation) are ineﬀ ective (Einhäupl et al 2010).

The duration of secondary prevention with anticoagulants is an important issue. In patients with a transient prothrombotic condition, a 3–6-month period of oral anticoagulation aiming for an international normalized ratio (INR) of 2–3 seems adequate. In idiopathic CVT, secondary prevention is generally recommended for a peri-

od of 6–12 months. In hereditary defects like deﬁ ciency of antithrombin III, protein C or protein S, activated protein C resistance/factor V Leiden mutation, prothrombin G20210A mutation, and rarer defects including heparin cofactor II deﬁ ciency (HC II), plasminogen or tissue plas- minogen activator deﬁ ciency (TPA), elevated plasmino- gen activator inhibitor-1 (PAI-1), and dysﬁ brinogenemia, as well as in positive antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibodies), indeﬁ nite anticoagulation should be considered at least in patients with recurrent CVT. The role of von Willebrand factor (factor VIII) and methylene tetrahydrofolate reductase mutation (hyperhomocysteinemia) is still unclear.

Angiologic and Anatomic Aspects

Digital subtraction angiography (DSA) has been the gold standard in diagnosing CVT for many years. In rare cases, for instance in case of equivocal MR and CT ﬁ ndings or if a prolonged vessel drainage has to be proven in cortical vein thrombosis, DSA still serves as the reference method. A lack of contrast ﬁ lling in the veins or sinuses is the main diagnostic sign. Diﬃ culties may be encountered because of the great variability of venous anatomy. The ability of DSA to assess dynamic aspects such as the delayed emptying of venous vessels and to detect collateral venous pathways in the sinus and veins (the latter called corkscrew veins) further underlines its diagnostic relevance. However, the invasiveness of DSA limits its use in daily clinical practice.

MR and CT techniques have currently replaced DSA in most institutions. MRI not only allows evaluation of parenchymal lesions, e.g., focal or global edema, infarction, and bleeding, but also visualization of the thrombus itself. T2* susceptibility-weighted sequences in combination with MR venography are currently the most reliable way to detect the thrombus, an occluded dural sinus, and especially a thrombosis in an isolated cortical vein (Fellner et al 2005, Selim et al 2002). Considering the signal intensities in the T1- and T2-weighted images, MRI is able to assess the age of a thrombus over time (Connor and Jarosz 2002). In the ﬁ rst few days the aﬀ ected sinuses ap- pear isointense on T1 and hypointense on T2-weighted images. After 5 days signal is increased in both T1- and T2-weighted images, making the thrombus more evident. In the chronic state, after 1 month, variable signal patterns may be present. FLAIR images should, however, be interpreted cautiously. In low ﬂ ow vessels, for example, in the nondominant TS, high signal intensity instead of a ﬂ ow void may appear, leading to the false-positive diagnosis of CVT (Klingebiel et al 2007). Gadolinium administration, similarly to contrast-enhanced CT, shows a vessel wall enhancement surrounding the thrombus and is also useful in detecting a chronic thrombus in a hypoplastic TS. Similarly to DSA, TOF-MRA is able to detect ﬁ lling de- fects in veins and sinuses. Because of its ﬂ ow dependen- cy, however, venous vessels with low ﬂ ow velocities or an alternating ﬂ ow may not be visualized. Cases in which a nondominant TS is not visualized and which may be confounded with thrombotic occlusion are again of major concern. As a left-sided dominance of the TS is found in only ~25% of cases, the question of thrombosis often rises

426 Case 29 Cerebral Venous Thrombosis

with regard to the left sinus (Ayanzen et al 2000). Contrast-enhanced MRA is more reliable and sensitive in the assessment of normal and obstructed venous vessels but should also take into account physiologic and anatomic diﬀ erences between the right and left TSs (Farb et al 2003, Klingebiel et al 2007).

MRI has also been used to study recanalization and its inﬂ uence on clinical outcome. Follow-up TOF-MRA in 33 patients demonstrated that recanalization occurs within the ﬁ rst 4 months but not thereafter. Thromboses of the SSS reopened in almost all cases (98%) while 42% of TS thromboses remained occluded (Baumgartner et al 2003). Similar results were observed in 37 patients studied by Stolz and coworkers. Most complete vessel normalization already occurred during the patient’s hospital stay (41%). After 6 months a complete recanalization had occurred in 51%. A partial recanalization was demonstrated in 19%, and in 30% the vessel remained occluded. A late recanalization between 6 and 12 months was observed in only one patient. Notably, the recanalization pattern was not correlated with clinical outcome (Stolz et al 2004).

Unenhanced CT can be of diagnostic value. In severely aﬀ ected patients, a focal or generalized brain edema or typical parenchymal bleeds may be present and can be indirectly suggestive of venous congestion. In up to 50% of cases the “cord sign,” i.e., direct thrombus visualization, can be found, comparable to the dense media sign in MCA occlusion. It may be present within any vein or sinus, depending on its location and extension, as was the case in our patient (Goldberg et al 1986). Isolated cortical vein thrombosis still present as a diagnostic challenge, in which unenhanced multislice CT (≤1 mm slice thickness) may prove useful in directly visualizing the small hyperdense cortical vein. If contrast agents are used, the “empty delta sign” can be found in SSS thrombosis in up to 50% of cases. The thrombus itself is spared but contrast enhancement is seen in the vessel wall surrounding the thrombus. A major pitfall can be an early bifurcation of the SSS in both TS. CTA depicts venous pathology in patients with CVT demonstrating ﬁ lling defects preferentially in the coronal, sagittal, or transverse plane depending on the site of CVT (Klingebiel et al 2002, Majoie et al 2004). Its main advantage is the speed of the procedure and its major ﬂ ow independence, which probably decreases the risk of false-positive ﬁ ndings sometimes observed in low ﬂ ow venous vessels using MR techniques. In two comparative studies with MR techniques CTA was shown to be at least equivalent. However, cortical vein thrombosis was not considered, which might be better visualized with MRI (Khandelwal et al 2006, Linn et al 2007). As in all present techniques, variations in the intracranial venous anatomy and properties of venous hemodynamics have to be taken into account to avoid false-positive interpretations. Plain CT and CT in bone window setting may allow visualizing the presence of a normal or narrowed sigmoid notch plate. In suspected CVT with absent TS and/or SiS, a wide sigmoid notch strongly argues in favor of thrombosis. A missing or rather small sigmoid notch plate has been referred as positive sigmoid notch sign (Chik et al

2012). Independent of the imaging technique applied one should be familiar with the numerous anatomic variants present in the venous vasculature. Of note, arachnoid

granulations seen on contrast-enhanced CT and MRI may be confused with dural sinus disease (Leach et al 1996).

Since the mid-1990s ultrasound has also been used to investigate patients with CVT by assessing venous collateral pathways, but not by visualization of the thrombus itself (Stolz et al 2002a, Valdueza et al 1999a). Its importance has gradually decreased over time with the increasing availability of MRI, MRA, and CTA techniques. However, whenever the latter are not available, venous transcranial color-coded duplex sonography (TCCS) analysis might be able to provide fast valuable diagnostic information. For example, if TCCS revealed intracranially increased venous but normal arterial ﬂ ow velocities in a young female patient with headaches and a ﬁ rst focal epileptic ﬁ t, CVT is the rather likely diagnosis. Then the only remaining diﬀ erential diagnosis is an arteriovenous ﬁ stula which has to be considered and ruled out (for further reading on ﬁ stula, see Case 34). In arteriovenous an- gioma typical arterial feeders with high ﬂ ow velocity and low pulsatility should be expected (for further reading on angioma, see Case 4, Case 32, and Case 40).

Because of the absence of valves in the intracranial venous system, ﬂ ow may follow the direction of need and any vein might serve as a collateral vessel. The size of the vessel, its ability to dilate, and the extent of total collateral ﬂ ow determine whether or not an increase in velocity occurs, which can subsequently be detected by ultrasound. TCCS has clear advantages over the TCD approach owing to its better anatomic orientation. For further discussion on venous ultrasound anatomy, see also Chapter 2, “Special Venous Anatomy and Ultrasound Anatomy.” In 20% of cases with CVT, however, no direct or indirect signs of compromised venous circulation may be seen (for further reading of ultrasound pattern in CVT, see Chapter 5, “Cerebral Venous Thrombosis” under “Venous Pathology”).

In our patient the aﬀ ected right TS was not visualized despite good insonation conditions. Hypoplasia of the right TS is rare and a missing signal may therefore be suggestive of an occlusion. Furthermore, the high left TS ﬂ ow velocity, clearly above the normal range, was also indicative of contralateral occlusion. The deﬁ nitive sonographic prove of this assumption, however, was the reappearing right TS ﬂ ow signal and the decreasing left TS ﬂ ow ve- locity during the course of the anticoagulation. The increased ﬂ ow velocities in the BVR and DMCV indicated an additional ﬂ ow obstruction of the SSS. Here a retrograde ﬂ ow from the bridging veins can be assumed which diverted the blood ﬂ ow into the deep veins, draining into the straight sinus and from there into the open left TS.

Finally, the value of a PI measurement needs a comment: The PI is at best a rough estimator of intracranial pressure (ICP). In a large study of 290 head trauma patients with ICP recording, the diagnostic value of PI in assessing ICP and CPP was limited. Only in patients with an ICP >35 mm Hg was PI indicative of raised ICP and extreme PI values may therefore favor decision for invasive ICP monitoring in these patients (Zweifel et al

2012). Another study reported that a PI >1.26 was associated with ICPs >20 cm H2O measured during lumbar puncture with a sensitivity and speciﬁ city of 81.1% and

96.3%, respectively (Wakerley et al 2015).

Case 30

Multilocular Extra- and Intracranial Stenoses and Occlusions

427

Clinical Presentation

A 41-year old woman presented to a district general hospital because of transient episodes of numbness in the left face and hand as well as left-sided blurred vision. There she underwent cerebral MRI and MR angiography (MRA). She was subsequently commenced on aspirin and 3 weeks later referred to our department for further clinical evaluation. No ultrasound examination was performed. The medical history revealed migraine, smoking, and alcohol misuse. There was no known arterial hypertension and she did not take any medication. On admission, her neurologic examination was normal.

Initial Neuroradiologic Findings (Day 1)

Cerebral MRI on admission to the district general hospital showed multiple signal abnormalities in the right hemisphere, consistent with internal border zone infarction (BZI). Contrast-enhanced extracranial MRA revealed vessel wall irregularities in the carotid arteries and occlusion of the left external carotid artery (ECA). Intracranially, time-of-ﬂ ight (TOF) MRA demonstrated a patent ﬂ ow signal in the left distal internal carotid artery (ICA) and absent ﬂ ow signals in the right M1 middle cerebral artery (MCA), and A1 anterior cerebral artery (ACA) segments. On T2-weighted images, however, a signal void of the right M1-MCA segment was clearly visible indicating patency of the MCA (Fig. B30.1, Fig. B30.2, Fig. B30.3, Fig. B30.4).

Suspected Diagnosis

Recurrent left-sided sensory transient ischemic attacks (TIAs) presumed to be of hemodynamic origin because of suspected pathology of the right MCA. Unresolved vessel status of the left distal ICA.

Questions to Answer by Ultrasound Techniques

• Were there real occlusions of the right M1-MCA and A1-ACA segments?

• Was there evidence of a distal occlusion of the asymptomatic left intracranial ICA?

• Were there signs of atherosclerosis or vasculitis?

Initial Neurosonologic Findings (Day 20)

Extracranial Duplex Sonography

B-mode sonography revealed left-accentuated severe atherosclerotic vascular changes with iso- to hyperechoic plaques, especially in the carotid bulbs. No ﬂ ow sig- nal was seen in the left ECA. Color-mode image of the left proximal ICA demonstrated a lumen reduction of ~40–50% caused by hypoechoic material. The ﬂ ow sig- nal in this area was regular (ﬂ ow velocity 115/58 cm/s). A markedly reduced ﬂ ow velocity was seen in the right ICA (ﬂ ow velocity 24/11 cm/s). Assessment of the verte- bral arteries (VAs) and right ECA revealed normal ﬁ ndings (Fig. B30.5, Fig. B30.6, Fig. B30.7).

Transcranial Duplex Sonography

Raised ﬂ ow velocities were found in the left-sided carotid siphon (ﬂ ow velocity 228/94 cm/s) and proximal M1-MCA segment (ﬂ ow velocity 221/131 cm/s). The distal MCA seg- ments on the left side revealed a mild poststenotic ﬂ ow pattern. A marked, slightly turbulent, and poststenotic ﬂ ow pattern was seen in the left A1-ACA segment which seemed to supply both A2 segments (ﬂ ow velocity 132/69 cm/s). The anterior communicating artery (ACoA) could not be detected. The left posterior cerebral artery (PCA) was almost normal with only slightly increased velocities. The right proximal M1-MCA segment demonstrated a turbulent ﬂ ow with increased velocity (ﬂ ow velocity 161/74 cm/s). The M2 branches revealed a distinct poststenotic ﬂ ow pattern. No right A1-ACA segment was detected. Raised ﬂ ow veloc- ities were found in the right P1- and P2-PCA segments indicating leptomeningeal collateralization (ﬂ ow velocity 159/88 cm/s). No ﬂ ow signal was seen in the left ophthal- mic artery (OA) while the right OA ﬂ ow was antegrade. Unsuspicious Doppler spectra were seen within the VAs and the basilar artery (BA) (Figs. B30.8–B30.15; see also

Videos

B30.1 and B30.2).

428 Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions

Conclusion

Severe atherosclerosis in the extracranial segments of the brain-supplying arteries with a left-sided proximal ICA stenosis of ~40–50% (low grade) and left ECA occlusion. Intracranially, left-sided high-grade tandem stenosis of the ICA siphon and proximal M1-MCA, together reaching hemodynamic relevance. On the right side, a hemodynamically relevant proximal M1-MCA stenosis and A1-ACA occlusion or aplasia was assumed. Blood supply to the right MCA territory via the ipsilateral ICA and leptomeningeal PCA anastomoses. Supply of the right ACA territory assumed to be via cross-ﬂ ow from the contralat- eral A1-ACA segment.

Conventional Angiography (Day 22)

Digital subtraction angiography (DSA) was performed to further analyze ﬂ ow pathways and to consider therapeu- tic options. It conﬁ rmed a left-sided moderate extracranial ICA stenosis and occlusion of the ECA as well as a left-sided intracranial ICA siphon and M1-MCA stenosis. Blood supply of both ACA territories was provided via the left A1-ACA segment. On the right side the A1-ACA and M1-MCA segments seemed to be occluded. During the late arterial sequences of the right ICA projection, however, a distinct temporal branch and a prominent insular M2 branch became visible. Abnormal dilated lenticulostriate vessels corresponding to a vascular collateral network were seen adjacent to the aﬀ ected main vessels. Left VA in- jection revealed a marked collateral ﬂ ow to the right MCA territory via leptomeningeal collaterals from the right PCA. In summary, the right-sided intracranial vessel status was evaluated as a near-occlusion of the right M1-MCA segment with collateralization of the MCA territory via the right PCA and right A1-ACA occlusion with collateralization via the contralateral ACA (Figs. B30.16–B30.21).

Fig. B30.22 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries at this stage.

Clinical Course (1)

The multilocular extracranial and intracranial pathology was attributed to atherosclerosis on the basis of the known heavy smoking and alcohol misuse and newly diagnosed hypercholesterolemia and hyperhomocysteinemia.

During the ﬁ rst few days in the hospital the patient had further mild clinical events with sensory disturbances of the left hand while her blood pressure was slightly elevated. Several days later she developed new recurrent contralateral symptoms—a severe right-sided brachiofacial paresis and global aphasia—each lasting 20–30 minutes. She was then referred to the stroke unit for further monitoring and blood pressure control. Despite a systolic blood pressure of 200 mm Hg achieved by dopamine infusion she ﬁ nally developed severe akinetic mutism. Follow-up MRI

1 day later revealed a new left-sided internal BZI, larger than on the right side. Extracranial ce-MRA and intracranial TOF-MRA showed no signal in the left common carotid artery (CCA), ICA, ECA, and ACA and a weak signal in both MCAs (Fig. B30.23, Fig. B30.24, Fig. B30.25).

Questions to Answer by Ultrasound Techniques

• Was there a real complete occlusion of the left carotid arteries?

• What is the vessel status of the right side?

• Was there permanent near-occlusion of the right M1-MCA segment?

Follow-up Neurosonologic Findings (Day 29)

Extracranial Duplex Sonography

The lumen of the left ICA and CCA was still visible. The ﬂ ow pattern of the left ICA had changed, revealing now a high-resistance ﬂ ow signal with a low and short systolic ﬂ ow and completely absent diastolic ﬂ ow, suggestive of distal ICA occlusion below the OA origin (Fig. B30.26). The left ECA signal remained absent. Flow signals in the right carotid arteries remained unchanged. Flow velocities in the VAs were increased.

Transcranial Duplex Sonography

No ﬂ ow signal was detected in the left distal ICA. The turbulent ﬂ ow pattern of the left MCA remained unchanged, but ﬂ ow velocities had decreased (ﬂ ow ve- locity 81/46 cm/s). Also the ﬂ ow velocity of the left A1- ACA segment was found to be lower than before and the poststenotic ﬂ ow pattern had become more prominent if compared with the ﬁ rst ultrasound examination (ﬂ ow ve- locity 53/33 cm/s). Raised ﬂ ow velocities were now found for the ﬁ rst time in the left P1-PCA segment (ﬂ ow velocity 190/99 cm/s). Distinct turbulences could be detected in the left posterior communicating artery (PCoA) indicating collateral function and blood supply toward the anterior circulation. Correspondingly, a raised ﬂ ow velocity but no turbulent ﬂ ow was now found in the BA (ﬂ ow veloc- ity 208/106 cm/s) (Fig. B30.27, Fig. B30.28, Fig. B30.29, Fig. B30.30, Fig. B30.31; see also Video changed ﬂ ow patterns were seen in the right MCA and OA.

Conclusion

Progressive vessel pathology with distal occlusion of the left ICA and inadequate collateralization via the left PCoA. Unchanged right-sided vessel status with near-occlusion of the M1-MCA segment.

B30.3). Un-

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