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239Discussion

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.

is accepted in all countries which permit the use of technical conﬁ rmatory testing; however, as it is an invasive technique, most guidelines recommend DSA only if it has a potential therapeutic consequence and not solely for brain death diagnosis. To date, neurosonologic examination is approved for documentation of cerebral circulatory arrest, e.g., in Germany, Switzerland, Austria, Canada, and the United States. A survey reported that 71 of 226 German neurologic and neurosurgical departments used ultrasound regularly as a conﬁ rmatory test (Wijdicks 2002). More recently, CTA has been accepted in some countries, including France, Switzerland, Austria, and Germany, but not in Canada or the United States. In Switzerland, MRI and MR angiography (MRA) are also accepted.

In summary, there is widespread variation between

countries regarding the preconditions for the clinical determination of brain death. Diﬀ erences exist between concepts of brainstem death (UK) and total brain death (other European countries and North America) as well as the approved technical conﬁ rmatory tests. In our case, brain death could not formally be diagnosed, as the ancillary ultrasound test was performed before clinical testing, which is not permitted according to the above mentioned guidelines for diagnosis of total irreversible loss of all brain function. During initiation of the formal testing, the patient died of a cardiac arrest. Therefore, we would like to stress that—to avoid any risk of false-positive evaluations—existing guidelines must always be complied with, even if this leads to instances where formal brain death diagnostics cannot be completed.

Angiologic and Anatomic Aspects

A precondition for brain circulatory arrest is the severe mismatch between systemic blood pressure and ICP.

Cessation of blood ﬂ ow only occurs if the ICP exceeds the systemic blood pressure with a resulting perfusion pressure of zero or less. The following four diagnostic approaches, which have, so far, been accepted in several countries, will brieﬂ y be discussed.

Digital Subtraction (Catheter) Angiography

Angiography was the ﬁ rst technique used to assess cerebral circulatory arrest and dates back over 50 years (Wertheimer et al 1960). Since then, angiographic techniques have been developed and improved (to the currently used DSA), but the diagnostic principle has remained unchanged. More speciﬁ cally, a selective ar- terial contrast injection in both internal carotid arteries (ICAs) and both vertebral arteries (VAs) is performed. Provided that a suﬃ cient systemic blood pressure is present (>80/>60 mm Hg mean blood pressure in adults/ children), lack of contrast ﬁ lling during radiographic monitoring conﬁ rms ﬂ ow cessation. This applies to the following vessel segments of the anterior circulation: extracranial ICA or intracranial supraophthalmic ICA or MCA and ACA oﬀ shoots. In the posterior circulation, contrast usually stops at the entrance of the skull—i.e., the V3–V4 segment of the VA. Taken together, these ﬁ ndings conﬁ rm circulatory arrest as long as no paren- chymal and venous ﬁ lling is observed. Example angio- graphy images, not related to the case presented here, are shown in Fig. B7.11 and Fig. B7.12. This technique has the advantages that its diagnostic sensitivity and speciﬁ city are high and the corresponding false-positive rate is virtually zero. However, arterial puncture and wire placement are invasive measures and can only be performed in the catheter laboratory, which requires t r a n s p o r t i n g a c r i t i c a l l y i l l p a t i e n t .

Fig. B7.11 DSA in a patient with cerebral circulator y arrest in the anterior circulation. Selective contrast ﬁ lling of the ICA: (A) pos- terior–anterior projection plane, (B) lateral projection plane. Note the tip of the catheter in the sub-basal ICA (solid arrow). Carotid contrast stops at the proximal carotid siphon (dashed arrows) ﬁ lling only the ophthalmic artery and related vessels of the face (dotted arrow).

Fig. B7.12 DSA in a patient with cerebral circulatory arrest in the posterior circulation (A) and in a healthy individual (B) for comparison. Selective contrast ﬁ lling of the right vertebral artery: (A) Flow cessation at the proximal V4-VA segment (dashed arrow), (B) regular V4-VA contrast ﬁ lling (dashed arrow). Missing BA contrast in A, regular BA contrast with ﬁ lling (dotted line arrow) and of cerebellar and posterior cerebral arteries in B. In A note the faint contrast ﬁ ll- ing of arterial anastomoses toward the extracranial neck arteries (arrow).

240 Case 7 Cerebral Circulatory Arrest

Perfusion Scintigraphy

The ﬁ rst observations of brain death determined by “isotope angiography” were reported by Goodman and coworkers (1969). Currently, the technique is applied as either planar or multiplanar scintigraphic imaging by single-photon emission CT (SPECT). The basis for these techniques is the intravenous injection of a validated radioactive tracer, e.g., Tc-99m hexamethylpropyleneamine oxime (HMPAO). The tracer distribution in the brain can then be analyzed (by planar or 3D analysis) and compared with patterns of the abdomen or thorax (Sinha and Conrad 2012). Provided that suﬃ cient systemic blood pressure is present (for values see “Digital Subtraction (Catheter) Angiography” above), a circulatory arrest is diagnosed if no radioactive tracer signal is found in the brain. Example images, not related to the present case, are shown in Fig. B7.13).

This technique has the advantage that it is both standardized and noninvasive. However, its availability is limited and requires the patient to be moved to a specialized center. Moreover, the procedure is time-consuming with, for example, a recommended time delay between tracer application and perfusion assessment of up to 2 hours. Additionally, patient positioning may be hindered by necessary life support equipment, thereby resulting in impaired image acquisition. However, more importantly, the diagnostic reliability of brainstem perfusion cessation (i.e., the range of brainstem size within the technique’s spatial resolution limits) has not been thoroughly studied (Sinha and Conrad 2012). This might explain some false-positive cases with absent blood ﬂ ow on radio- nuclide angiography but persistent residual brainstem function (Flowers and Patel 1997). The ﬁ ndings also e m p h a s i z e t h e n e e d t o a d h e r e t o t h e e x i s t i n g b r a i n d e a t h diagnosis guidelines, which demand clinical patient evaluation before proceeding to other ancillary testing.

Fig. B7.13 HMPAO–SPECT in a patient with total cerebral circulatory arrest. Note the preserved nuclide accumulation in the skull and face (“hot nose sign”) but missing signal from the brain itself. (Image kindly provided by Dr. Buchert, Department of Nuclear Medicine, Charité – Universitätsmedizin Berlin, Germany.)

CT Angiography

CTA has recently been accepted in several countries as a further additional ancillary test for the detection of cerebral circulatory arrest. The ﬁ rst reports of missing vessel CT contrast enhancement in patients with brain death date from the late 1970s (Rappaport et al 1978). However, the basis for accepting CTA as a measure of cerebral circulatory arrest derives from more recent studies (Dupas et al 1998, Wels cheho ld et al 2013 a, 2013b ). The basic pri ncip le governing the use of CTA as a diagnostic parameter is the observation of the arrival of a contrast bolus in the intracranial arteries (assessed by spiral CT). Provided that a suﬃ cient systemic blood pressure is present (mean arterial pressure >60 mm Hg), a lack of intracranial contrast enhancement and concomitant contrast enhancement of extracranial arteries (e.g., the temporal artery) conﬁ rms cerebral circu- latory arrest. However, with respect to contrast detection, CTA seems far more sensitive than DSA. A comparison of patients in whom both DSA and CTA was performed showed that some patients had positive CTA contrast (e.g., in the M1-MCA or A1-ACA) but a lack of contrast in the corresponding DSA (Dupas et al 1998). This ﬁ nding is further complicated by the fact that the number of contrast-positive vessel segments largely depends on the timing of the scan in relation to the bolus application. An early-phase CT scan will show fewer vessels with positive contrast whereas a late-phase CT will shows more (Frampas et al 2009, Welschehold et al 2013b). The study of Frampas and coworkers (2009) is one of the papers frequently cited in relation to the formal acceptance of CTA. In their study, 105 patients were included with a clinical diagnosis of brain death according to current clinical standard criteria. Applying a 7-point score, derived from earlier work (Dupas et al 1998), CTA sensitivity was 62.8% using signal analysis in pericallosal arteries, cortical MCAs, internal cerebral veins, and the vein of Galen. The authors then replaced the above evaluation in the same patient group with a 4-point score (both cortical MCAs and both internal cerebral veins only) which resulted in a diagnostic sensitivity of 85.7%. In our opinion, it seems questionable to improve sensitivity by avoiding evaluation of vessels with positive contrast. As the study inclusion criterion was clinical brain death syndrome, which does not necessarily equal cerebral circulatory arrest (percentage of patients with preserved blood ﬂ ow in this group not known), the above suggestion seems problematic. Finally, data regarding the posterior circulation, i.e., the basilar artery (BA) and VAs, was not provided. A further CTA approach analyzed vessel opaciﬁ cation in distal segments of the MCA, ACA, BA, and the V4-VA segments (Welschehold et al 2013b). The authors described this contrast ﬁ ll- ing as “stasis ﬁ lling,” but they did not oﬀ er a solution for a clear diﬀ erentiation between residual brain perfusion and the stasis ﬁ lling phenomenon. Only solving this issue will ﬁ nally clarify the vessel segments that can safely be analyzed without risking the generation of false-positive CTA results. To date, there is one published case report of a patient diagnosed with cerebral circulatory arrest using CTA who had an antegrade intracranial blood ﬂ ow on follow-up transcranial Doppler (TCD) (Greer et al 2009). However, the patient was apparently hemodynamically

unstable during CT and had been subsequently stabilized

prior to TCD. This raises doubts as to whether this can be considered a true false-positive case.

A recent Cochrane review analyzing data from 8 studies and 337 patients concluded that: “The available evidence cannot support the use of CTA as a mandatory test, or as a complete replacement for neurologic testing, in the management pathway of patients who are suspected to be clinically brain dead” (Taylor et al 2014). They also underline the need for further studies. The ideal study design for this would be to analyze CTA results in selected patients with assured cerebral circulatory arrest, determined by one of the other accepted ancillary tests for assessment of the cerebral circulation.

In conclusion, CTA is a promising technique which is minimal invasive and fast (once the patient has been transported to the CT-scanner). Further studies should clarify whether CTA is prone to false-positive results, e.g., in cases of slow and delayed blood ﬂ ow to the brain. Subsequently, the exact technical requirements for the scanner and its imaging quality, the optimal time point for scanning after administration of an intravenous contrast bolus, and the number and location of the vessel segments to be evaluated should be deﬁ ned.

Ultrasound

The ﬁ rst application of ultrasound in patients with suspected cerebral circulatory arrest was the use of ﬂ ow analysis in the common carotid arteries (CCAs) (Despland and de Crousaz 1974). The development of TCD, some 10 years later, quickly facilitated a more widespread application of the technique as a direct assessment of (1) the associated intracranial ﬂ ow pat- terns, and (2) underlying pathophysiologic processes (Harders 1986, Ropper et al 1987). If the ICP rises above normal values, the ﬂ ow pattern of intracranial vessels will change from low resistance to high resistance with reduced diastolic ﬂ ow and increased pulsatility. If ICP equals the diastolic blood pressure, diastolic ﬂ ow will cease while the systolic ﬂ ow component persists. A fur- ther ICP increase up to systolic blood pressure values leads to three characteristic pathognomonic ﬂ ow pat- terns which correlate with catheter-angiographic loss of brain perfusion (Hassler et al 1988, 1989, Ropper et al 1987, van Velthoven and Calliauw 1988). Example images, not related to the present case, are shown in Fig. B7.14. The three patterns are:

• Alternating ﬂ ow, where the sum of anterograde and ret-

rograde ﬂ ow leads to a net zero ﬂ ow which correlates well with DSA-determined circulatory arrest.

• Systolic spikes, deﬁ ned as pure systolic ﬂ ow of less

than 200 ms duration and less than 50 cm/s peak s y s t o l i c ﬂ ow velocity. In these cases it is thought that the retrograde ﬂ ow component is either too slow to be depicted or the integrated high-pass ﬁ lters prevent their detection: ﬁ lters should therefore be set as low as possible.

• Total absence of ﬂ ow signals (Hassler et al 1988).

Fig. B7.14 Example images of ﬂ ow patterns detected by ultra- sound consistent with circulatory arrest.

These three grades of cerebral circulatory arrest correlate well with the extracranial ﬂ ow interruptions visible in DSA (Hassler et al 1989). How can these patterns be explained if DSA shows complete absence of ﬂ ow? Although this has not been formally resolved, there is a possible explanation. The most plausible hypothesis is that the percussive eﬀ ect of heartbeats with ultrasound moves the stagnant blood column back and forth, which is facilitated by the elasticity of the arterial walls. If both ﬂ ow portions are equal, contrast should not advance into vessel segments with this ﬂ ow pattern. As pressure increases, the intravascular blood is either squeezed out or consolidated so that even the alternating movement is prevented, resulting in a systolic spike pattern (Ducrocq et al 1998a, Topcuoglu and Arsava 2013).

Alternating ﬂ ow signals in circulatory arrest can also be seen in the extracranial portion of brain-supplying arteries. However, ﬂ ow within the extracranial ICA can be altered if blood ﬂ ows via the ophthalmic artery (OA) into the eye and face. In these instances, a dramatically reduced systolic ﬂ ow and a persisting diastolic ﬂ ow sig- nal can be seen. The CCA usually shows an antegrade ﬂ ow feeding the external carotid artery (ECA) (von Reutern and von Büdingen 1993). A similar pattern may be observed in the extracranial VA if residual ﬂ ow occurs at the V2–V3 level into communicating neck arteries (see also Fig. B7.11 and Fig. B7.12).

These ﬂ Doppler or duple

ow patterns can be detected using either

asound systems. Though duplex

x ultr ultrasound allows easier assignment of the exact vessel segments during insonation, both techniques need to be adjusted for the detection of low ﬂ ow velocities. For Doppler systems, this comprises a pulse repetition frequency (PRF) as low as possible, the deactivation of wall ﬁ lters, the enlargement of the Doppler sample volume (10–15 mm) and the increase of system power and gain. For duplex ultrasound systems, the color window needs additional optimization by choosing a small color window, using a low color window PRF, and increasing the color gain.

241Discussion

242 Case 7 Cerebral Circulatory Arrest

According to the Task Force Group on cerebral death of the Neurosonology Research Group of the World Federation of Neurology’s 1998 recommendations (Ducrocq et al 1998b), a circulatory arrest may be diagnosed by ultrasound if the following criteria are fulﬁ lled (but note that these might not be legally applicable or might be modiﬁ ed in diﬀ erent countries):

• A combined extracranial and intracranial ultrasound

analysis has to be performed.

• The above described ﬂ ow signals have to be present

over a time period of 30 minutes.

• Transcranially, all main stems of the brain-supplying

arteries have to be studied.

• At least two of them must have the alternating ﬂ ow de-

scribed above if the remaining vessel signals are missing.

• The suspected diagnosis has to be conﬁ rmed by extrac-

ranial ultrasound analysis of ﬂ ow in the CCA, ICA, and VA (Ducrocq et al 1998b).

The last requirement leads to a considerable number of false-negative results. As discussed before, antegrade OA ﬂ ow and distal VA extracranial anastomoses may lead to antegrade extracranial ICA and VA ﬂ ow patterns and not to the expected patterns of circulatory arrest.

Lack of a transcranial signal is not a safe sign of circulatory arrest, as this ﬁ nding might result from a missing bone window. Only the disappearance of a formerly observed ﬂ ow signal in combination with typical extracra- nial ﬂ ow patterns is acceptable. Although not mentioned in the 1998 criteria, Doppler and duplex ultrasound—like any of the aforementioned techniques that can conﬁ rm circulatory arrest—also require presence of a suﬃ cient systemic blood pressure (mean arterial pressure >60 mm Hg). The recommended time interval (30 minutes) between repeated assessments results from ﬁ ndings that showed that very short time periods of alternating blood ﬂ ow might not lead to conﬁ rmation of brain death. Two infants with a short diastolic ﬂ ow reversal survived the condition. In one, the ﬂ ow pattern was caused by a status epilepticus which was acutely treated. The second was caused by a decompensating intracranial tumor which was surgically removed (Chiu et al 1994). This corresponds well with experiences from cardiac arrest where irreversible loss of total brain function is observed if cerebral ischemia periods last 10–15 minutes (Ducrocq et al 1998a). The number and location of vessel segments to be documented varies remarkably between diﬀ erent countries. In some, the above criteria are applied. Others consider the occurrence of the typical ﬂ ow patterns in MCA and BA suﬃ cient. An obligatory CCA insonation does not seem sensible, as ﬂ ow toward the undisturbed ECA will lead to a pulsatile but antegrade systolic and diastolic ﬂ ow. For guidelines currently applicable in Germany, see Fig. B7.15.

Transcranial ultrasound has been used to assess c e r e b r a l c i r c u l a t o r y a r r e s t i n s e v e r a l s t u d i e s . A m e t a - a n a l y s i s i n 2 0 0 6 s u m m a r i z e d d a t a f r o m 1 0 p u b l i cations concerning the validity of ultrasound (Monteiro et al 2006). In accordance with data from the subcommittee of the American Academy of Neurology (Sloan et al 2004), they reported a sensitivity varying between 89% and 95% but a speciﬁ city of only 99%. The latter

Fig. B7.15 Vessel segmen ts re quir ed to be ins onated and docu mented with ﬂ ow patterns of cerebral circulatory arrest according to the fourth revision of the guidelines from the German Medical A s s o c i a t i o n ( B u n d e s ä r z t e k a m m e r 2 0 1 5 ) i f D o p p l e r u l t r a s o u n d (A) or duplex ultrasound (B) is used.

r e s u l t s f r o m t w o c a s e s . T h e ﬁ rst of these was a 61-year- old woman with traumatic brain injury who had oscillating ﬂ ow patterns in both MCAs and VAs, and the BA, with a total absence of brainstem reﬂ exes but “weak respiratory movements” during apnea testing (Hadani et al 1999). A subsequent perfusion SPECT was performed, which showed absence of cerebral blood ﬂ ow, and a fol- low-up apnea test demonstrated apnea. However, the patient was hypothermic at the time of ultrasound analysis which should have been an exclusion criterion (see “Clinical Aspects” above). The second reported case was a 34-year-old man with traumatic brain injury who fulﬁ lled the clinical criteria of brainstem death, in whom the authors found the typical TCD pattern of circulatory arrest while the EEG was not yet isoelectric (van Velthoven and Calliauw 1988). However, the authors only presented a recording of a singular vessel and did not comment on whether they found conﬁ rmatory signals in all brain-supplying arteries. Also, information regard-

erenc

ing the time diﬀ

e between ultrasound recording, EEG, and the results of a repeated conﬁ rmatory TCD af- ter 30 minutes was not available.

Other studies with questionable ﬁ ndings either stud- ied the patient only once while in unstable hemodynamic conditions (Nebra et al 2001), failed to perform clinical testing before the ultrasound study, and accepted any three positive vessels over 3 minutes as circulatory arrest (Dosemeci et al 2004), or performed single time measurements of the MCAs only (Kirkham et al 1987, Newell et al 1989, Powers et al 1989).

All of the above cases emphasize the importance of exact application of the current guidelines for diagnosis of brain death to avoid true evaluation errors. In our opinion, the above discussion shows that there are in fact no published true false-positive TCD cases and that the speciﬁ city can therefore assumed to be 100%.

However, if ultrasound is used to prove cerebral circulatory arrest, several further potential pitfalls that may lead to misinterpretation have to be considered: First, a patent acoustic temporal bone window is mandatory.

243Discussion

A missing transtemporal bone window might be substituted by transorbital insonation. Usually the applied insonation energy is therefore set higher than the usually accepted MI for the insonation of the eye (Lampl et al 2002, Soldatos et al 2010). By adding transorbital access, only 1.5% of the patients analyzed had a complete absence of all intracranial vessel signals (de Freitas and André 2006). A new approach is to improve insonation conditions by means of echo contrast-enhanced ultrasound. One study (n = 102) reported that a missing or insuﬃ cient transtemporal bone window was observed in 27% of TCD cases. Intravenous application of 2.5 mL SonoVue reduced this number to 3% (Welschehold et al 2013a). The waveforms of circulatory arrest described earlier will then be seen more easily if present after microbubble arrival.

Second, misinterpretation of ultrasound results may arise from a persisting intracranial ﬂ ow despite the presence of a clinically or EEG-conﬁ rmed brain death (false-negative result). Ogata et al (1988) reported that patients with a complete loss of brain stem function may show a persisting blood ﬂ ow toward both cerebral hem- ispheres. De Freitas and André (2006) found that a 17.4% of cases with clinically diagnosed brain death had persistent blood ﬂ ow. Patients with an open skull fracture, leading to a reduced ICP, might present with persistent cerebral ﬂ ow despite the total irreversible loss of brain function. Additionally, EEG might show persistent bioelectric activity, at least within the ﬁ rst few hours following clinical brain death (van Velthoven and Calliauw 1988).

False-negative results may delay the diagnosis of brain death, whereas false-positive results would be fatal and must not occur.

Extracranial duplex sonography alone has been used in one study analyzing extracranial blood volume ﬂ ow. A total cerebral blood volume ﬂ ow below 100 mL/min, assessed as the sum of volume ﬂ ows in both ICA and VA (for details see Chapter 3, “Cerebral Blood Flow V o l u m e ” u n d e r “ P a r a m e t e r s o f C e r e b r a l H e m o d y n a m ics”), was found in all patients clinically diagnosed with brain death. The authors suggested that this method might be applied in cases with an absent transtemporal bone window (Schöning et al 2005). However, this approach has not been further validated. The detection of alternating ﬂ ow in all four extracranial brain-sup- plying arteries could also be used for indirect exclusion of the presence of an intracranial antegrade ﬂ ow. If applicable, this would permit sonographic conﬁ rma- tion of cerebral circulatory arrest independent of the presence of a bone window. However, the approach has also so far not been validated and therefore cannot be recommended.

In conclusion, both TCD and TCCS are easily available techniques, usable at the bedside, that can be conﬁ dently applied to diagnose cerebral circulatory arrest provided that the transcranial insonation conditions are suﬃ cient. Their use is limited in any form of skull defects and in very young children with open fontanels, as these conditions are likely to lead to false-negative r e s u l t s .

244

Case 8

Basilar Artery Occlusion in Bilateral Intracranial V4 Vertebral Artery Stenosis

Clinical Presentation

A 56-year-old man was admitted to a district general hospital with acute left-sided hemiparesis, double vision, and mild nausea. The symptoms resolved except for an incomplete right oculomotor palsy. During the following hours he experienced ﬂ uctuating neurologic symptoms of transient left-sided hemiparesis, double vision, and reduced consciousness, each episode lasting for a few minutes. He had no known vascular risk factors.

Initial Neuroradiologic Findings

Cranial CT (CCT) showed normal ﬁ ndings without early signs of ischemic infarction, but CT angiography (CTA) demonstrated a distal basilar artery (BA) occlusion. Furthermore, severe calciﬁ cations in the distal intracranial vertebral artery (VA) on both sides were seen (not shown).

Suspected Diagnosis

Multiple transient ischemic attacks in the vertebrobasilar artery territory due to distal BA occlusion of unknown origin.

Conventional Angiography (Day 1)

On the basis of the above ﬁ ndings, digital subtraction angiography (DSA) was performed which conﬁ rmed the occlusion of the BA, beginning at the mid-basilar level. Collateralization of the posterior circulation was seen from the left internal carotid artery (ICA) via the left posterior communicating artery (PCoA). In addition, bilateral high-grade stenosis of the distal VA was conﬁ rmed (Fig. B8.1).

An artery-to-artery embolism originating from one of the VA stenoses was considered to be the cause of the BA occlusion. Six hours after symptom onset intra-arterial thrombolysis via the left VA was performed; administration of 50 mg recombinant tissue plasminogen activator (rt-PA) followed by 20 mg abciximab led to complete BA recanalization. Furthermore, balloon dilatation of the left high-grade VA s ten o si s w as p er fo rm ed b ut n o i nt ra l um in al st en t wa s inserted (Fig. B8.2). The right VA stenosis was left untreated.

Clinical Course (1)

The procedure was uneventful and subsequent blood pressure was kept within the high-normal range. The residual neurologic symptoms resolved completely and no new ischemic events occurred. Laboratory testing revealed an elevated HbA diabetes mellitus. One day after thrombolysis, a control CT scan was performed which disclosed a small right cerebellar infarction within the superior cerebellar artery (SCA) territory (Fig. B8.3). Secondary stroke prevention was started with aspirin, and the asymptomatic patient was discharged.

Six weeks later the patient was admitted to our department for the ﬁ rst time with repetitive transient epi- sodes of vertigo, nausea, and gait disorder.

consistent with the diagnosis of

Questions to Answer by Ultrasound Techniques

• Was there reocclusion of the BA after intra-arterial

thrombolysis?

• What was the postinterventional status of the left VA

and of the known high-grade right distal VA stenosis?

Initial Neurosonologic Findings (Day 42)

Extracranial Duplex Sonography

B-mode sonography showed mild atherosclerotic vascular changes in both carotid arteries without evidence of stenosis. Both V2-VA segment diameters were within the normal range (left, 4.5 mm; right, 3.2 mm). Doppler spectrum analysis revealed an obviously increased pulsatility in the left V2-VA segment and only mild signs of increased pulsatility on the right V2-VA suggestive of distal

ﬂ ow obstruction (Fig. B8.4, Fig. B8.5, Fig. B8.6, Fig. B8.7).

Transcranial Duplex Sonography

Transtemporal insonation was impossible because of a bilaterally absent temporal bone window. The transforaminal insonation showed turbulent ﬂ ow signals and increased ﬂ ow velocities in both V4-VA segments,

245Initial Neurosonologic Findings (Day 42)

Fig. B8.1 DSA, left VA injection, posteroanterior view. Left VA-V4 stenosis (arrowhead) and BA occlusion starting at the mid- basilar region (arrow). (Courtesy of Prof. Faiss, Asklepios Fachklinikum Teupitz, Teupitz, Germany.)

Fig. B8.3 Unenhanced CT, axial plane. Circumscribed right c e r e b e l l a r i n f a r c t i o n w i t h i n t h e S C A t e r r i t o r y ( a r r o w ) . ( C o u r t e s y o f Dr. Faiss, Asklepios Fachklinikum Teupitz, Teupitz, Germany.)

Fig. B8.2 DSA, left VA injection, posteroanterior view. Complete recanalization of the BA after intra-arterial thrombolysis. Diminished left V4-VA stenosis after balloon dilatation (arrows). (Courtesy of Prof. Faiss, Asklepios Fachklinikum Teupitz, Teupitz, Germany.)

V2-VA-L

Fig. B8.4 Extracranial duplex, longitudinal plane. Left V2-VA diameter 4.5 mm.

reaching a peak systolic ﬂ ow velocity of 175 cm/s (in- sonation depth 61 mm) on the left side and 169 cm/s (insonation depth 67 mm) on the right. The BA had a low ﬂ ow velocity (37/18 cm/s) but an otherwise nor- mal ﬂ ow pattern (Fig. B8.8, Fig. B8.9, Fig. B8.10; see also Video

B8.1).

Conclusion

Bilateral left-pronounced intracranial VA stenoses (>50%) without evident hemodynamic relevance. Restenosis of the left VA after balloon dilatation. No evidence of reocclusion or stenosis of the BA.

246 Case 8 Basilar Artery Occlusion in Bilateral Intracranial V4 Vertebral Artery Stenosis

V2-VA-R

Fig. B8.5 Extracranial duplex, longitudinal plane. Right V2-VA diameter 3.2 mm.

V2-VA-R

V2-VA-L

Fig. B8.6 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the left V2-VA with increased pulsatility (ﬂ ow velocity 46/11 cm/s, PI = 2.8). Note the mild retrograde ﬂ ow component indicating relevant distal obstruction.

V4-VA-L

Fig. B8.7 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right V2-VA with mildly increased pulsatility (ﬂ ow velocity 72/14 cm/s, PI = 1.7).

V4-VA-R

Fig. B8.9 TCCS (t rans foram inal approach) . Turbu lent an d increa sed

ﬂ ow in the right V4-VA (ﬂ ow velocity 169/70 cm/s).

Fig. B8.8 TCCS (t rans foram inal approach) . Turbu lent an d increa sed

ﬂ ow in the left V4-VA (ﬂ ow velocity 175/79 cm/s).

Fig. B8.10 TCCS (tran sforamina l appro ach) . Nor mal ﬂ ow in the BA.

Fig. B8.11 CTA, coronal MIP: 4 weeks after thrombolysis and

left-sided balloon dilatation a persisting bilateral intracranial VA stenosis with massive local calciﬁ cation hindering graduation of stenoses can be seen (arrowheads). Note that there is a signal loss in the right distal V4-VA which is caused by an elongated vessel course and not by a distal vessel occlusion.

Neuroradiologic Findings

MRI could not be performed because the patient experienced severe claustrophobia. Cerebral CT did not show any new ischemic lesion. CTA conﬁ rmed the bilateral intracranial VA stenoses with severe calciﬁ cation in this area (Fig. B8.11).

Clinical Course (2)

During the next few days the patient experienced further recurrent episodes of vertigo and nausea which were closely related to episodes of low blood pressure. Clopidogrel was added as a second antiplatelet agent and attempts were made to keep the blood pressure within the upper normal range. Interventional treatment with stent placement was discussed but refused by the patient. During 3 years of follow-up with dual antiplatelet therapy, no new ischemic event occurred and the neurosonologic ﬁ ndings remained unchanged.

Final Diagnosis

Successful intra-arterial thrombolysis in distal BA occlusion probably caused by artery-to-artery embolism from bilateral calciﬁ ed intracranial VA stenoses >50%. Suspect- ed additional hemodynamic transient ischemic attacks (TIAs) originating from the vertebrobasilar circulation.

247Discussion

Discussion

Clinical Aspects

The patient was a 56-year-old man with bilateral intracranial VA stenoses. An artery-to-artery embolism originated from one of these stenoses and subsequently led to a distal BA occlusion. Intra-arterial thrombolysis was successfully performed and only a small right-sided cerebellar infarct within the SCA territory remained. The case represents a special pathologic constellation within the vertebrobasilar territory because of the bilaterally aﬀ ect- ed V4-VA segments.

According to reports of several stroke databases, ischemic events of the posterior circulation account for ~20% of strokes. Only 1% of all strokes are due to BA occlusion (Bogousslavsky et al 1988, Gulli et al 2013, Moulin et al 1997, Vemmos et al 2000). The New England Medical Center Posterior Circulation Registry is the largest relevant database comprising prospectively collected data of 407 patients (Caplan et al 2004). Of these, 59% had a stroke, 24% TIA followed by stroke, and 16% had a TIA only. Ischemic strokes of the posterior circulation were caused by embolic events in 40% of cases when considering the single most likely mechanism. Of these, 60% were thought to be of cardioembolic origin, artery-to-artery embolic events originating from the posterior circulation accounted for 35%, and a mixed cause in the remaining 5% of cases. Large-artery occlusive lesions causing stroke (32%), vessel branch occlusion (14%), migraine (3%), and others (10%) were the next relevant causes (Caplan et al

2004). A tendency of embolism due to large-artery atherosclerotic disease was reported in a large registry including 8,057 patients. Here atherosclerosis was assumed to be the main cause in posterior circulation ischemia in 35%, followed by cardioembolism in 18%, and small-vessel disease in 13% (Labropoulos et al 2011).

Stenoses of the posterior circulation are predominantly found at the VA origin followed by the BA and the intracranial VA. Within the intracranial VA they are most frequently found, near the origin of the posterior inferior cerebellar artery (PICA). Bilateral stenoses, as in our case are a frequent ﬁ nding (Bogousslavsky et al 1988, Caplan 1983, Müller-Küppers et al 1997). The New England Medical Center Posterior Circulation Registry reported clinical and radiologic ﬁ ndings of 42 patients (9.8%) with bilateral intracranial VA involvement. Of these, 18 had a bilateral stenosis, 8 had a bilateral occlusion, and 16 had a unilateral occlusion and a contralateral stenosis. Only 6 patients (14%) had isolated bilateral intracranial VA pathology. The others presented in addition occlusive vascular lesions in the BA (69%), the extracranial VA (43%), and also in the ICA (26%). Most of the stenoses were of atherothrombotic origin (Shin et al 1999). Distal BA occlusion is mostly caused by embolism. Atherosclerotic BA occlusions are usually located in its proximal and middle segment.

Similar to the anterior circulation, microembolic signals can be detected in the BA preferentially in severe intracranial VA stenosis (Hwang et al 2012).

248 Case 8 Basilar Artery Occlusion in Bilateral Intracranial V4 Vertebral Artery Stenosis

Our patient revealed severe calciﬁ cations of both VA seen on conventional CT and also in the bone window. Despite the easy and frequently detectable pathology, clinical interest started late. Analyzing 175 ischemic stroke patients and 182 controls the highest prevalence of calciﬁ cation was seen in the ICA artery in 80.4%, followed by the VA in 35.6%. Stroke patients revealed a higher prevalence of calciﬁ cation than controls (92.6% versus 76.4%) (Chen et al 2007). Looking only for VA calciﬁ cations in 449 consecutive patients with stroke, more than half of them (54.6%) had visible calciﬁ cations. Calciﬁ cations in the VA were associated with higher age, larger calciﬁ ed areas, and history of TIA and/or stroke (Pikija et al 2014).

In cases of chronic and slowly progressing occlusive processes, patients with distal VA stenoses develop different collateral pathways. Collateralization may occur from the anterior circulation via the PCoA or the posterior circulation via the cerebellar arteries through leptomeningeal pathways from the PICA to the SCA, and anterior spinal artery. However, often this is not suﬃ cient, which may lead to impaired perfusion in the dependent brain territories. Consequently, patients present with recurrent stereotyped TIAs. Vertigo, dysarthria, ataxia, and double vision are the most frequent symptoms, which may be aggravated by orthostatic or antihypertensive therapy (Caplan 1996). Shin and coworkers (1999) found that 81% of patients in the group with TIAs had bilateral VA pathology; 38% of the TIAs were isolated events, and the remainder occurred before or after manifestation of stroke. In most TIAs a hemodynamic cause was suspected (Shin et al 1999). As in our case, transient vertigo and ataxia were the most frequently found clinical symptoms. The main components of the vestibulocerebellar system, located in the cerebellum and brainstem, derive their blood supply from the distal VA via penetrating branches and the PICA and are quickly aﬀ ected by a reduced antegrade perfusion. However, the diagnosis of a hemodynamic impairment caused by steno-occlusive processes within the vertebrobasilar circulation requires careful clinical assessment as well as good imaging analysis. In fact, it seems to be less frequently present than previously assumed. In the New England Posterior Circulation Register a hemodynamic ischemia, predominantly caused by bilateral intracranial VA stenosis, was reported in 13 of 407 patients (Savitz and Caplan 2005).

If a completed stroke occurs, the infarct pattern depends on the site of the vascular pathology. Medullary infarctions or infarcts of the PICA territory are observed if the stenotic process is located proximal to, or directly at the origin of the PICA. Ischemia within the BA, SCA, and posterior cerebral artery (PCA) territory occur more often in stenotic processes distal to the PICA branch. Artery-to-artery embolic events from atheromatous plaques located in the intracranial VA may also result in distal patterns of infarction. In our patient, a VA-derived embolus caused a distal BA occlusion with clinically ﬂ uc- tuating signs of a “top-of-the-basilar-syndrome” (Caplan 1980, Mehler 1989). In cases of persisting occlusion this may lead to ischemic infarctions in the upper pons, mid-

PCA territory. However, the extent may vary, as can be seen in our patient who only suﬀ ered a partial SCA infarc-

tion. From this we can assume that although the occlusion began at the mid-basilar level, it must have extended to the head of the BA. We can also conclude that our patient’s clinical symptoms were indicative of distal BA involvement, as they consisted mainly of a mesencephalic dysfunction (transient third nerve palsy and ﬂ uctuation in consciousness). Because of the ﬂ uctuating symptoms, lack of ischemic signs on cerebral CT, and veriﬁ cation of the BA occlusion by DSA, an intracranial thrombolysis was performed which led to complete recanalization 6 hours after the onset of his symptoms. Furthermore, balloon dilatation of the left high-grade VA stenosis was performed.

The treatment recommendation in thromboembolic occlusions of the BA is similar to those in the a n t e r i o r c i r c u l a t i o n a n d i n c l u d e s i n t r a v e n o u s t h r o m bolysis with recombinant tissue plasminogen activator (IV rt-PA), intra-arterial thrombolysis, and endovascular t h r o m b e c t o m y .

For treatment decision, the clinical severity (assessed by the NIHSS score) plays an important role. However, the NIHSS score has some limitations if applied to ischemic stroke of the posterior circulation. Strokes within the anterior circulation usually attain higher scores because of cortical signs and/or motor deﬁ cits. Posterior circulation ischemia often scores lower as cranial nerve deﬁ cits and ataxia without paresis are weighted lower. Despite relatively lower NIHSS scores, patients with posterior circulation stroke often show a worse outcome (De Marchis et al 2011, Sato et al 2008).

The recently published Third International Stroke Trial (IST 3) reported on thrombolysis using IV rt-PA within a 6-hour time window. It showed an improvement in the functional outcome but no reduction in mortality. A limiting factor, however, might have been that only 246 of the 3,025 patients included suﬀ ered from stroke in the posterior circulation (Sandercock et al 2013).

Untreated BA occlusion is a neurologic emergency, mostly with a fatal outcome. This is why available treatment strategies have also been applied beyond the therapeutic time windows consented for the anterior circulation. Lindsberg and colleagues applied systemic rt-PA thrombolysis in patients with vertebrobasilar occlusion up to 12 hours after disease onset in sudden disturbance of consciousness and tetraparesis and up to 48 hours after disease onset in those with gradually increasing brainstem symptoms (Lindsberg et al 2004). In this series including 43 patients with a BA occlusion, 52% showed a BA recanalization. The mortality after 3 months was 40%, and 22% of patients achieved a good clinical outcome, being independent in all functions of daily living. In patients with a stuttering course and no early infarct signs, the time window for intra-arterial and systemic thrombolysis may even be extended at least to up to 48 hours after onset of symptoms (Lindsberg and Mattle 2006). In a large prospective study evaluating 184 consecutive patients with angiography-proven BA occlusion and subsequent IV rt-PA treatment followed by concomitant full-dose heparin administered within up to 48 hours achieved good clinical outcomes in 50% of cases, independent of the time onset of treatment. Factors associated with a poor outcome were higher age and bad clinical status, a

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