In patients who experience an ischaemic stroke while on effective anticoagulation, intravenous thrombolysis (IVT), is currently contraindicated due to concerns that the risk for major bleeding events, particularly intracranial hemorrhage (ICH), is particularly increased. Current guidelines do not recommend IVT in patients with acute ischaemic stroke who have taken a NOAC within 48 hours before the event (1). However, this assumption is not evidence-based. Up to 20% of all strokes occur while on effective NOAC treatment (2). As the spectrum of indications for NOACs is continuously expanding, it can be assumed that this proportion of patients who are withheld IVT on the basis of this paradigm will continue to grow and thus become even more relevant.

Previous studies did not indicate a substantial risk for bleeding events in thrombolysed patients who are taking a NOAC  (3, 4). In a current retrospective, international multi-center study led by the colleagues from Bern (Switzerland) and Heidelberg (Germany), Meinel et al. analysed data from patients who received IVT between 2008 and 2021 and had taken a NOAC within 48 hours before symptom onset of stroke (5). As control cohort, patients treated with IVT but not under effective anticoagulation were included, most of them recruited in the Thrombolysis in Ischaemic Stroke Patients (TRISP) collaboration. When available, the exact NOAC intake time before stroke was documented and categorised according to within 12 hours, 12-24 hours, or over 24 hours. Information on the respective regimen was also collected, i.e., to what extent NOAC plasma levels were measured or NOAC were antagonised before IVT. The primary endpoint was the occurrence of a symptomatic ICH (defined as worsening by 4 NIHSS points) within 36 hours after IVT. Secondary endpoints were any ICH on follow-up imaging and a favorable functional outcome according to a modified Rankin Scale of 0-2, which was assessed center-based at 90 days via a clinical or telephone visit. (5)

There were 832 patients with NOAC treatment and 32375 controls included. In the NOAC group, patients were older (79 vs. 72 years) and had higher stroke severity (median NIHSS 11 vs. 9), prevalence of proximal vessel occlusion (59% vs. 33%), and atrial fibrillation (90% vs. 25%). Dabigatran was the most common anticoagulant used (41%), followed by rivaroxaban (31%), apixaban (20%), and edoxaban (8%). Among NOAC-treated patients, antagonisation (idarucizumab for dabigatran) was performed in 30% and NOAC plasma levels were measured in 27%. In the NOAC group, the rate of symptomatic ICH was 2.5% compared with 4.1% in controls. The adjusted odds ratio (OR) for symptomatic ICH was 0.57 (95% confidence interval : 0.36-0.92). In prespecified sensitivity analyses using the different time intervals, this result was consistent, with the limitation of small number of cases. Patients who received NOAC but in whom neither plasma level measurement nor antagonisation could be performed (n=355) still had a nominally decreased risk of symptomatic ICH (aOR: 0.66 (95% CI: 0.35-1.25)) but an increased OR for any ICH (aOR: 1.58 (95% CI: 1.16-2.14)), although the precision of these estimates was quite low. (5)

The occurrence of secondary end points did not differ considerably between groups. (5)

This important study again plausibly challenges the paradigm of contraindication of thrombolysis by NOAC treatment. Contrary to the expectation, the risk of symptomatic ICH due to thrombolysis was even significantly reduced under existing NOAC treatment, which may be explained by improved thrombolytic properties and reduced blood-brain barrier disruption. (5)

The most important limitation of the study is its retrospective design and a probable selection bias: the treating colleagues will have selected suitable patients having low risks for hemorrhagic transformation of stroke in their routine practice. Subgroup analyses have shown similar trends but had too little statistical power to provide reliable estimates.

While a randomised-controlled trial on this topic is unlikely to ever be planned for financial and logistical reasons, a prospective registry of appropriate size seems to be warranted in order to change the current practice in favor of the many NOAC-treated patients. A particularly interesting group are patients for whom the practitioners are unaware of NOAC use, as no selection bias would be expected here.

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References:

1. Berge E, Whiteley W, Audebert H, De Marchis G, Fonseca AC, Padiglioni C, et al. European Stroke Organisation (ESO) guidelines on intravenous thrombolysis for acute ischaemic stroke. European Stroke Journal. 2021;6(1):I-LXII.
2. Seiffge DJ, De Marchis GM, Koga M, Paciaroni M, Wilson D, Cappellari M, et al. Ischemic Stroke despite Oral Anticoagulant Therapy in Patients with Atrial Fibrillation. Ann Neurol. 2020;87(5):677-87.
3. Seiffge DJ, Hooff RJ, Nolte CH, Béjot Y, Turc G, Ikenberg B, et al. Recanalization therapies in acute ischemic stroke patients: impact of prior treatment with novel oral anticoagulants on bleeding complications and outcome. Circulation. 2015;132(13):1261-9.
4. Xian Y, Federspiel JJ, Hernandez AF, Laskowitz DT, Schwamm LH, Bhatt DL, et al. Use of Intravenous Recombinant Tissue Plasminogen Activator in Patients With Acute Ischemic Stroke Who Take Non-Vitamin K Antagonist Oral Anticoagulants Before Stroke. Circulation. 2017;135(11):1024-35.
5. Meinel TR, Wilson D, Gensicke H, Scheitz JF, Ringleb P, Goganau I, et al. Intravenous Thrombolysis in Patients With Ischemic Stroke and Recent Ingestion of Direct Oral Anticoagulants. JAMA Neurology. 2023.

Neck pain and headache are part of the common clinical picture of cervical arterial dissections. In general, vertebral artery dissections more frequently present with neck pain, as opposed to internal carotid artery dissections, in which headaches are slightly more common.¹ Accompanying neurological deficits may develop after a delay that can range from hours to days, or even weeks.^2–4 The Horner syndrome together with pain is almost pathognomonic of carotid artery dissection.⁴

Even though isolated cephalalgia as the sole presentation of cervical artery dissection has been reported, patients might not be recognized when they don’t have neurological deficits. In a case series of 20 patients with a cervical arterial dissection presenting only with neck pain or headache, patients often had a history of hypercholesterolemia, smoking, or migraine with or without aura.⁵ More often than not, pain was reported as severe and patients required analgesics.^4,6

With regard to the carotid artery, the patient may report a headache that is ipsilateral to the dissection, non-pulsatile, severe, and with a sudden onset.^2–4 Occasionally, the headache may have migraine-like characteristics, but its occurrence in patients over the age of 30, with recent history of minor trauma and with no family history of migraine should alarm the clinician.⁷ Cervical artery dissection may also present with symptoms similar to a ‘status migrainosus.’⁸ Migraineurs will usually describe the pain as notably distinct from other episodes, however there are exceptions.⁵ Besides, cluster-like presentations have also been described.⁴

In vertebral artery dissection, cephalalgia is often occipital and unilateral (also ipsilateral to the causative injury), although diffuse and frontal pain have also been described. In terms of quality of the pain, there is a high variability, from sharp to constrictive or diffuse pain.^3,5 Some cases may have thunderclap characteristics that require a differential diagnosis with a subarachnoid hemorrhage.² A pressing quality and posterior localization may cause the pain to be mistaken for tension-type headache.⁶ A characteristic that can prove to be a hint indicating vertebral artery dissection is the headache’s variation with movements of the neck (both exacerbation and relief may occur on flexion or extension).⁹ Migraine characteristics are more rare in vertebral artery dissection, although they have been described, with visual aura mimics (scintillating scotomas) being attributed to emboli in the occipital lobe.¹⁰

In conclusion, cervical artery dissections should be considered in the differential diagnosis of neck pain and headache in the emergency department. Given the delay that may occur in between the development of other characteristic neurological findings, an open mind can mean time bought in terms of adequate treatment for patients presenting with cephalalgia as the only symptom.

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References:

1. Debette S, Grond-Ginsbach C, Bodenant M, et al. Cervical Artery Dissection Ischemic Stroke Patients (CADISP) Group. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology, 2011;Sep 20;77(12):1174-81.
2. Mokri, B Headaches in cervical artery dissections. Current Pain and Headache Reports, 2002;6(3), 209–216.
3. Silbert PL, Mokri B, Schievink WI. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Neurology, 1995 Aug;45(8):1517-22.
4. Biousse V, D’Anglejan-Chatillon J, Massiou H, et al. Head pain in non-traumatic carotid artery dissection: a series of 65 patients. Cephalalgia, 1994 Feb;14(1):33-6.
5. Arnold M, Cumurciuc R, Stapf C, et al. Pain as the only symptom of cervical artery dissection. J Neurol Neurosurg Psychiatry. 2006;77(9):1021.
6. Matsumoto H, Hanayama H, Sakurai Y, et al. Investigation of the characteristics of headache due to unruptured intracranial vertebral artery dissection. Cephalalgia. 2019;39(4):504-514.
7. Mirza Z, Hayward P, Hulbert D. Spontaneous carotid artery dissection presenting as migraine-a diagnosis not to be missed. Emerg Med. 1998;15:187-199.
8. Sainz AR, Calle IA, Ontanon JM, et al. Bilateral Carotid Dissection Presenting as Status Migrainosus: All That Glitters Is Not Gold. J Med Cases. 2014;5(9):502-504.
9. Kim JG, Choi JY, Kim SU, et al. Headache characteristics of uncomplicated intracranial vertebral artery dissection and validation of ICHD-3 beta diagnostic criteria for headache attributed to intracranial artery dissection. Cephalalgia. 2015;35(6):516-526.
10. Morelli N, Mancuso M, Gori S, et al. Vertebral artery dissection onset mimics migraine with aura in a graphic designer. Headache. 2008 Apr;48(4):621-4.

Periprocedural factors influencing functional outcomes after mechanical thrombectomy (MT) for large vessel occlusion strokes (LVOS) are increasingly recognised. Besides multiple studies on ship strategies and anaesthesia, the management of blood pressure (BP) and blood pressure targets during and after MT has extensively been studied.

BP targets prior to MT are based on current guideline recommendations taking into account data on intravenous thrombolysis. Penumbra and collateral artery perfusion are the basis for higher systolic BP (SBP) targets prior to MT and during IVT (150-180 mmHg) (1) (2). Expert opinions suggest no use of antihypertensives prior successful recanalization up to SBPs of >200 mmHg, while in bridging thrombolysis scenarios the upper SBP limit should be around 180 mmHg to avoid intracerebral hemorrhage (ICH) (3).

Optimal management of BP after successful reperfusion is less clear. Retrospective studies indicated different BP trajectories after MT with higher and lower mean BPs associated with higher mortality rates and unfavorable outcomes (4) (5). In these studies, LVO patients with high or high to moderate BP trajectories (mean BPs >140 mmHg) had significantly higher odds of unfavorable functional outcomes and increased risk of symptomatic ICH (6). One study identified increased SBP 24h after MT to be a predictor of early neurological deterioration, poorer 90 day modified Rankin Scale scores and higher rates of symptomatic ICH (7). In addition, BP variability and the amount of BP peaks have been identified as independent predictors for unfavorable functional outcomes (7) (8).

After publication of this data, the question remained if elevated BP after MT is an epiphenomenon or causative linked to unfavorable outcome. It has been speculated, that increased BPs contribute to capillary leak, reperfusion injury and higher odds of symptomatic ICH and hemorrhagic transformation due to impaired cerebrovascular autoregulation in the ischemic vessels. To clarify the causative link, one large, retrospective analysis including data from 10 comprehensive stroke centers found that BP reduction after successful MT within the first 24 hours was inversely correlated with functional outcomes, providing evidence for a therapeutical target (9). In the same population SBP goals of <140 mmHg after MT were associated with favorable functional outcomes, as well as lower odds of decompressive hemicraniectomy and symptomatic ICH compared to a SBP goal of <180 mmHg (10).

Concerning RCTs, one study including 324 patients in four MT centers, found no significantly different rates of ICH or mortality 16-24h after MT in two treatment groups with BP goals of 100-130 mmHg and 130-180 mmHg.(11) Another open-label, blinded-endpoint, randomized controlled trial at 44 tertiary-level hospitals in China including 802 patients after MT assigned patients in an intensive BP lowering- and less intensive BP lowering group. BP targets for the intensive group were <120 mmHg and less intensive group 140-180 mmHg, to be achieved within 1 hour and sustained 72 h after MT. This study was stopped due to persistent efficacy and safety concerns, as patients in the intensive BP lowering group were less likely to have favorable functional outcomes and had higher rates of early neurological deterioration and mortality (12).

Multiple studies are on the way to further provide more robust evidence for BP targets after MT. The Blood pressure After Endovascular Stroke Therapy (BEST-II, NCT04116112), Outcome in patients Treated with Intraarterial Thrombectomy- Optimal Blood Pressure Control (OPTIMAL_BP; NCT04205305), Invasive Control of Blood Pressure in Acute Ischemic Stroke After Endovascular Therapy on Clinical Outcomes (CRISIS I; NCT04775147) trials will compare various outcome parameters using SBP cut-off values of 140 mmHg (13).

Based on current evidence, it seems reasonable to aim for higher SBPs (140-180 mmHg) prior to MT and in patients with unsuccessful reperfusion (TICI 0 to 2a). This especially seems to be relevant in cases with concomitant extracranial stenosis, poor collateral status and intracranial arteriosclerotic disease (ICAD). After successful recanalisation (TICI 2b, 2c or 3), systolic BP targets of 120-140 mmHg seem to have beneficial effects (10) (14), while intensive BP lowering to SBPs <120 mmHg seems to have adverse effects on functional outcome and mortality rates (maybe particularly in Asian populations). Ongoing trials will help to further specify BP targets depending on the degree of recanalisation after MT, to optimise individualised treatment decisions.

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References:

1. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the AHA/ASA. Stroke . 50:e344., 2019.
2. Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. . N Engl J Med . 372:1019., 2015.
3. Biller J, Bulwa Z, Gomez CR, Morales-Vidal S. Stroke snapshot: Blood pressure management after acute ischemic stroke. . Pract Neurol (Fort Washington, Pa.) . March/April:13., 2019.
4. Prasad A, Kobsa J, Kodali S, et al. Temporal profiles of systolic blood pressure variability and neurologic outcomes after endovascular thrombectomy. . Eur Stroke J. . 7(4):365-375. , 2022 D.
5. Petersen NH, Kodali S, Meng C, et al. Blood Pressure Trajectory Groups and Outcome After Endovascular Thrombectomy: A Multicenter Study. . Stroke. . 53(4):1216-1225. , 2022 .
6. Anadani M, Orabi MY, Alawieh A, et al. Blood Pressure and Outcome After Mechanical Thrombectomy With Successful Revascularization. . Stroke. . 50(9):2448-2454., 2019 .
7. Katsanos AH, Malhotra K, Ahmed N, et al. Blood Pressure After Endovascular Thrombectomy and Outcomes in Patients With Acute Ischemic Stroke: An Individual Patient Data Meta-analysis. Neurology. . 98(3):e291-e301., 2022 .
8. Maier IL, Tsogkas I, Behme D, et al. High Systolic Blood Pressure after Successful Endovascular Treatment Affects Early Functional Outcome in Acute Ischemic Stroke. . Cerebrovasc Dis. . 24;45(1-2):18-25. , 2017 .

An unusual, sudden and severe headache, during the days, or even weeks, before bleeding event has been reported in 15% to 60% of patients with aneurysmal subarachnoid hemorrhage (aSAH). It is referred to as “warning leak”, “minor leak” or “sentinel headache” (SH)¹.

Clinical relevance of SH is a matter of debate. Some authors suggested an active diagnostic attitude towards patients experiencing an unusual headache, as it offers a means of improving the overall outcome in patients with aSAH, while others even questioned the existence of the SH, attributing its high incidence to a “recall bias”². Indeed, older studies assessing the prognostic value of SH^1,3,4 collected retrospective data, asking patients with aSAH whether they had experienced any episodes of acute, sudden-onset severe headache in the 2 weeks preceding the most recent bleeding event. Insofar, results might be altered by the foregone exclusion of cases with poor outcome and by the lack of clinical features to distinguish SH from other types of headache.

Most recent studies tried to overcome this diagnostic problem, showing that the concept of SH can be supported by using MRI techniques^5,6,7:

Firstly, using the susceptibility weighted imaging (SWI)⁵ and the quantitative susceptibility mapping (QSM)⁶, an advancement of the previous technique that provides quantitative maps. SWI and QSM may show the iron deposit caused by microbleeds of the aneurysm and correlated with the headache. They seem particularly effective in aneurysms of the middle cerebral arteries or posterior circulation, which do not have the limit of the skull-base bone artifacts.

Secondly, with the T1 weighted imaging (T1WI)-FLAIR mismatch⁷. It is defined as the presence of bright hyperintense subarachnoid blood (BHSB) in T1 images, although less widespread compared to the BHSB detected in FLAIR images. The BHSB of T1WI represents the subacute blood of the minor leak, while the BHSB of FLAIR images the subsequent re-bleeding.

Finally, with the aneurysm wall enhancement (AWE) of the Vascular Wall Imaging (VWI)⁸. It may predict symptomatic presentation (SH or III nerve palsy), growth or rupture of intracranial aneurysms (IA). It is associated with increased proinflammatory markers and might identify areas of increased vasa vasorum, neovascularization and macrophage infiltration. Hence, the AWE could be considered a surrogate biomarker of aneurysm instability, even in patients with SH and no minor leak.

In conclusion, these studies support the existence of SH . These studies also pointed out that SH could be caused by a minor bleeding from a leak of a berry aneurysm or by a warning inflammatory process that can precede the aSAH. Hence, in patients with unruptured IA whether the headache comes from the aneurysm might potentially be clarified.

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References:

1.F H Linn, E F Wijdicks, Y van der Graaf, F A Weerdesteyn-van Vliet, A I Bartelds, J van Gijn. Prospective study of sentinel headache in aneurysmal subarachnoid haemorrhage. Lancet. 1994 Aug 27;344(8922):590-3. doi: 10.1016/s0140-6736(94)91970-4.

2.K E Jakobsson, H Säveland, J Hillman, G Edner, S Zygmunt, L Brandt, L Pellettieri. Warning leak and management outcome in aneurysmal subarachnoid hemorrhage. J Neurosurg. 1996 Dec;85(6):995-9. doi: 10.3171/jns.1996.85.6.0995.

3.Jürgen Beck, Andreas Raabe, Andrea Szelenyi, Joachim Berkefeld, Rüdiger Gerlach, Matthias Setzer, Volker Seifert. Sentinel headache and the risk of rebleeding after aneurysmal subarachnoid hemorrhage. Stroke. 2006 Nov;37(11):2733-7. doi: 10.1161/01.STR.0000244762.51326.e7. Epub 2006 Sep 28.

4. Viarasilpa T, Ghosh P, Gidwani S, Lantigua H, De Marchis GM, Panyavachiraporn N, Schmidt JM, Lee K, Badjatia N, Agarwal S, Claassen J, Mayer SA. Prognostic Significance of Sentinel Headache Preceding Aneurysmal Subarachnoid Hemorrhage. World Neurosurg. 2020 Jul;139:e672-e676. doi: 10.1016/j.wneu.2020.04.097. Epub 2020 Apr 24. PMID: 32339738.
5. Wan Z, Meng H, Xu N, Liu T, Chen Z, Sun Y, Wang H. Clinical characteristics associated with sentinel headache in patients with unruptured intracranial aneurysms. Interv Neuroradiol. 2021 Aug;27(4):497-502. doi: 10.1177/1591019920971977. Epub 2020 Nov 4. PMID: 33148104; PMCID: PMC8580530.
6. Nakagawa D, Kudo K, Awe O, Zanaty M, Nagahama Y, Cushing C, Magnotta V, Hayakawa M, Allan L, Greenlee J, Awad IA, Carroll T, Torner J, Raghavan ML, Hasan DM. Detection of microbleeds associated with sentinel headache using MRI quantitative susceptibility mapping: pilot study. J Neurosurg. 2018 May 1:1-7. doi: 10.3171/2018.2.JNS1884. Epub ahead of print. PMID: 29799347; PMCID: PMC6773513.
7. Oda S, Shimoda M, Hirayama A, Imai M, Komatsu F, Shigematsu H, Nishiyama J, Hotta K, Matsumae M. Retrospective review of previous minor leak before major subarachnoid hemorrhage diagnosed by MRI as a predictor of occurrence of symptomatic delayed cerebral ischemia. J Neurosurg. 2018 Feb;128(2):499-505. doi: 10.3171/2016.10.JNS161964. Epub 2017 Feb 10. PMID: 28186448.
8. Raghuram A, Sanchez S, Wendt L, Cochran S, Ishii D, Osorno C, Bathla G, Koscik TR, Torner J, Hasan D, Samaniego EA. 3D aneurysm wall enhancement is associated with symptomatic presentation. J Neurointerv Surg. 2022 Jul 19:neurintsurg-2022-019125. doi: 10.1136/jnis-2022-019125. Epub ahead of print. PMID: 35853699.

As we welcome 2023, we look back on a year where the pandemic entered another phase and the long periods of physical distance ended in most parts of the world. Many stroke physicians and researchers experienced the interactivity and immersion of the in-person ESOC in Lyon, France. At the YSPR mentoring Workshop, young researchers presented their projects and received valuable feedback. The ESO Summer School in Birmingham, England, was also an exciting in-person gathering where young ESO members learned about current stroke practices and new research directions.

We are looking forward to another year of exciting conferences; ESOC 2023 will take place on May 24-26 as a fully onsite conference in Munich, Germany. If you are a young investigator, do not miss the opportunity to submit an abstract for the workshop describing a planned research study or an ongoing project. The selected applicants will give an oral presentation, followed by constructive assessment of the study’s design and advice on its future development by a senior invited investigator. The abstract submission deadline is 17 January.

In the past year, the YSPR committee met many new talented young physicians and researchers. We welcomed new members to our board and invited new bloggers to join the YSPR members to contribute to our ESO blog. You can already have a look to past blog posts in the ESO blog. We hope to continue this much appreciated collaboration in the new year.

We are also just launching the new “Young Reviewer Training Programme”, in collaboration with the European Stroke Journal (ESJ). More than 140 talented candidates have applied for this programme and we are looking very much forward to kick off very soon. The 10 selected candidates will start working on peer-reviews together with their dedicated mentors early next year.

The D2D programme also continued this year to exchange doctors between specialised stroke departments. You can read about their experience in the ESO blog. In 2023 the D2D programme will continue to help 10 young physicians and researchers interested in the stroke field. If this sounds like something you would like: applications for 2023 are now open.

In 2023, the YSPR will continue to promote the future of all young physicians and researchers across Europe. We will also continue to publish comments on new ESJ papers. For the latest stroke news, keep following us on the ESO blog and Twitter.

We would like to thank all members who have been participating in ESO initiatives for their dedication. Let us hope for the same level of hard work in 2023. We encourage all ESO members to stay informed about developments in various fields of stroke and to be open to new ideas and approaches, as these can help to inspire and motivate us to achieve our goals and make a positive impact in the world.

We wish everyone a very happy 2023!

I had a great opportunity to be a part of ESO’s D2D programme. I was hosted by Prof. Else Charlotte Sandset and her great team at Oslo University Hospital, Norway. My visit lasted for 10 days, and it was a blast. After I was introduced to the whole team, without further delay, the team started with their regular working duties. The working agenda includes a lot of team work and discussions about admitted patients and their follow–up, both seniors and juniors, as well as neurologists and radiologists. I think this is a great way of learning and exchange of opinions, which I would like to have more frequently in hospital I am working at. As meetings are done, we proceeded for regular rounds and check–ups of patients, but someone can ask where is fun in that?!

Do not forget this is a stroke unit, so there is always some adrenaline rush. Stroke code was run, and we proceeded further. With a pre–notification system, the stroke team is waiting prepared for the patient to come in. What’s even more exciting, is that people here are coming not just by ambulance, but with helicopter also, as was the case with this patient. The paramedic team is well prepared and has all important information about the patient, so nothing is missed, and there is no delay. Blood work is done on the site, and we have proceeded straight to the CT lab for CT, CTA and CT perfusion. This hospital has a policy “straight to the CT”, where intravenous thrombolysis, if the patient is eligible, is started as soon as the CT is done. This working pathway helps to reduce door–to–needle time quite a lot, and for this patient it took around 18 minutes for all to be done (come in, report, neurological examination, blood draw, transportation to the CT, doing CT and bolus of tPA). Dr. Advani, one of the young stroke  consultants, showed me how good simulation in hospital settings can improve so much quality of services provided by whole team, doctors and nurses. It is also an awarding experience for residents because they are being trained in the decision–making process, with feedback from seniors. I really liked this working path, and now thanks to this visit, I have the experience needed to introduce this to the stroke team in my hospital.

During my stay, I made a presentation about stroke care in Novi Sad and Vojvodina, where I come from. The whole team here in Oslo is well intended, so they had a few questions about organization back in my country, and a ton of suggestions on how can we improve our stroke care. It was a big scope of information and ideas, that even while I am writing this report, the other parts of my brain are thinking about how to perform and to implement many of those suggestions. Also, I met Dr. M. Ranhoff Hov and talked with her about how technology can help in pre-hospital management of patients and how it affects the outcomes. It was so inspiring, because I am very keen on technology in medicine.

The working week ended with a Zoom lecture by Dr. Marc Ribo, a neurointerventionalist from Barcelona, about endovascular treatment of intracranial stenoses. It has become a tradition in Oslo hospital to have “International Friday” in this way, and Dr. Sandset is personally “responsible” for this great idea and organization.

I cannot leave out the part about Oslo and Norway. Architecture and landscape are the first things that took my breath away as soon as I landed. Everything is so well organized. Oslo has a lot of museums, and many of them are dedicated to contemporary art, showing how this nation is accepting and nurturing art and history together. Communication in the city was no problem at all, because almost everyone speaks English really well. Norwegians are so kind, and always with a smile on their faces, that even if it’s cold outside, you always have warm reception. It felt like I never left Serbia, but… I have.

It was a great experience, and I think it should be experienced by everyone who has an interest in stroke. This way you can step up your knowledge, and pass on your experience to others and make further improvement back at home. At least, this is my plan. I would like to express my gratitude to ESO and to my host, Dr. Else Charlotte Sandset, for organization and effort.

It was a great pleasure to spend one week in the Neurology Department of Keppler University in Linz where I met the perfect team in stroke unit.

Under the supervision of Dr. Milan Vosco and his team, as a representative of the ESO EAST in Kyrgyzstan, I had a great chance to see with my own eyes how the stroke service and stroke management was organized in Upper Austria. During my visit, I had the opportunity to watch and participate in the doctor’s routine work in the emergency department, stroke unit, neurovascular sonography lab and neuroimaging department.

I spent the first days in the stroke department, which is located in the university hospital. Every morning began with a round table and discussion of patients and general plans. Next, the patients were examined in the ward round. I was also lucky to see how the emergency department works on duty day and even managed to admit patients with a possible stroke. The patient is admitted through the ambulance line and brought to the hospital, where a neurologist in the emergency room conducts an initial neurological examination and then sends for neuroimaging. While the initial examination is being carried out, nurses take blood tests for examinations. After neuroimaging, the patient is sent to the stroke unit. In the stroke department, from the very first days, active rehabilitation is carried out by a multidisciplinary team: ergotherapist, speech therapist and rehabilitator.

One day I spent in the neurocampus, in the stroke department, where I could see the organization of transportation and delivery of a patient with a stroke from a remote region by helicopter. This patient then underwent a thrombectomy procedure with a successful outcome.

I learned a many new key tips regarding stroke care, and will share with my colleagues and try to implement some of these in our stroke departments.

I would like to express my deepest gratitude to all the staff from the Neurology Department of Keppler University for their hospitality and courtesy (both professional and personal), with a special word of appreciation to Dr. Milan Vosko and Dr. Kateryna Kulyk.

I am very much honoured that the European Stroke Organization granted me for this Department to Department programme and I would like to thank the ESO for this brilliant opportunity to gained more knowledge in stroke management.

Infectious endocarditis might be one of the most challenging diagnoses in internal medicine, due to its polymorphic clinical picture. Infectious endocarditis can lead to neurological signs and symptoms, caused mostly by embolic events. The Duke criteria have become a great tool for evaluating clinical cases and classifying them into definite/possible/rejected cases of infectious endocarditis since the 1990’s¹. This evaluation helped clinicians in choosing further investigations and treatment.

However, times have changed and MRI is now an important imaging study and even neurologically asymptomatic patients can show various abnormalities on brain MRI. A study conducted in 2009 covered the subject of arterial brain embolisms in infectious endocarditis, comparing the neurological examination with the MRI results. Only 25% of the patients had neurological exam abnormalities consistent with a stroke, while MRI proved ischemic events in 80% of the patients².  Clinicians should be aware of the impact brought by brain MRI when it comes to ischemic events, considering that this could change the clinical course of the patients in terms of treatment, as embolic phenomena represent one of the Duke criteria.

Another study performed in France on a larger population showed similar results regarding the correlation between the neurological exam and clinically silent brain MRI lesions. Moreover, it was shown how performing cerebral MRI could change the course of treatment, due to the fact that it updated the diagnosis for 32% of the patients to possible/definite case of infectious endocarditis, considering the Duke criteria^3,4. Furthermore, there were 3 deaths of neurologically asymptomatic patients during the follow-up period and abnormal findings on cerebral MRI should raise concern in terms of further complications, such as recurrence or hemorrhagic transformation, despite the normal neurological exam³.

There is also another important concern regarding brain MRI abnormalities and that is the finding of cerebral microbleeds. These microhemorrhages are not included in the Duke (or the modified Duke) criteria and they are usually attributed to amyloid angiopathy or hypertensive vasculopathy, with characteristic patterns of distribution in the brain, based on the underlying microvascular changes⁵. Several studies have shown that infectious endocarditis can present with cerebral microbleeds at the MRI examination, also in asymptomatic patients⁴. Some of these studies have reported cerebral microbleeds as the most frequent brain lesion found in patients with infectious endocarditis^3,6. Taking these into account, the recognition of cerebral microbleeds as usual findings in infective endocarditis could also change the impact of brain MRI for patients with high clinical suspicion.

We can conclude that brain MRI is definitely an important tool in infectious endocarditis for patients with and without neurological signs. However, further studies are needed to describe MRI lesions and their sensitivity and specificity for the diagnosis of infectious endocarditis (especially since coexisting small vessel disease might cause similar radiological findings). Eventually, an updated list of criteria could include cerebral abnormalities seen on MRI, which might help us in an earlier diagnosis and treatment.

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References:

1. Li, J. S. et al. Proposed Modifications to the Duke Criteria for the Diagnosis of Infective Endocarditis. Clin. Infect. Dis. 30, 633–638 (2000).
2. Cooper, H. A. et al. Subclinical Brain Embolization in Left-Sided Infective Endocarditis: Results From the Evaluation by MRI of the Brains of Patients With Left-Sided Intracardiac Solid Masses (EMBOLISM) Pilot Study. Circulation 120, 585–591 (2009).
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