“Smoked or baked towel”. It was only after the third time repeating himself I finally realised what I was being asked “Small or big towel”. I was at the hotel gym reception; the thick Glaswegian accent was going to take some getting used to.

I arrived in Glasgow, disconcertingly sunny, concerned I may have caught the wrong train. It was the inaugural European stroke organisation conference, in its infancy after splitting from the European stroke conference. 2700 attendees, 160 scientific oral presentations, 1100 posters; this was clearly going to be a success.

The conference was arranged into parallel sessions run over three days divided into: general interest, focused clinical topics, focused research topics, care/patient organisation, scientific communications, teaching courses and industry supported symposia. With so many parallel sessions it is impossible to cover the whole conference, so I will present some personal highlights.

No other sub specialty within Neurology has accelerated as fast as vascular neurology over the past four years. The introduction of non vitamin K oral anticoagulants (NOACs) has changed the face of stroke prevention in atrial fibrillation (AF) and continues to do so. More recently the endovascular trials have caused a sea change in hyperacute stroke care, whilst intracerebral haemorrhage (ICH) understanding, management and prevention is also a burgeoning research topic. All three topics had major roles at the conference.

Endovascular treatment (thrombectomy) in addition to routine IV thrombolysis for major proximal anterior circulation occlusions was further confirmed as a new standard of care. Four positive endovascular trials were announced at the international stroke conference earlier this year in Nashville Tennessee, and ESOC continued the trend: two further trials were announced (ESCAPE and REVASCAT), whilst MR CLEAN and SWIFT PRIME released sub analysis of their trials.

In keeping with the four recently published endovascular trials both ESCAPE and REVASCAT were positive and strikingly similar. ESCAPE shows that endovascular thrombectomy is 2.6 times more likely to yield a good clinical outcome compared with tPA alone with a number needed to treat of 41 whilst REVASCAT odds ratio was 1.7 for the same outcome with a NNT of 6.2 Despite these excellent results and the very good recanalisation rates achieved in all the recent endovascular trials, a poor outcome (mRS 3-6) still remains prevalent. A shift in focus now turns to neuro-protective agents or other adjunctive strategies to salvage more penumbra.

NOACs continue to make headlines: a recent meta analysis showed that they are superior to VKA in preventing cardioembolic stroke whilst having markedly lower ICH risk (RR 0.49).3 Phase IV registry data for Dabigatran was presented showing very similar results to those seen in the RCT, suggesting RCT data is applicable to the “real world”.4 Lastly, a small case series from our team at Queen Square was presented comparing NOAC ICH with warfarin ICH: interestingly NOAC ICH cases had smaller haemorrhage sizes and better clinical outcomes when compared with warfarin ICH cases.

Despite only representing a small proportion of stroke, ICH is a major cause of stroke mortality. As such there was significant interest in this topic. The clinical dilemma of restarting oral anticoagulants (OAC) for AF prevention after ICH was the topic of two talks. A Danish registry of 1032 patients with follow up over 2.4 years revealed a lower incidence of ischaemic stroke (IS) (HR 0.37) and mortality (HR 0.37) for those who restarted OAC without an increase risk of major bleeding (HR 0.67). This data supports a similar finding by German group whose results were recently published in JAMA.5 Preliminary results from an unpublished multi-centre study revealed the marked variation in centres in restarting OAC in patients with AF after ICH (7%-72%). Clearly a randomised controlled trial (RCT) is needed, to this end the protocol for APACHE-AF was presented. More work is also needed to define subtypes of ICH (e.g. cerebral amyloid angiopathy, CAA) which may respond differently to exposure to antithrombotic drugs.

Further presentations on ICH included;

  1. Meta analysis on ICH cases in alteplase RCTs. Findings revealed a delay in treatment, increasing age and baseline NIHSS score was not associated with an increased odds of ICH although there was an absolute increase in ICH with increasing NIHSS scores.
  2. A sub analysis from INTERACT 2 shows a very interesting association between ICH risk and the temperature in the preceding 72 hours. Low temperatures (especially below 0) show higher risk of ICH. This was somewhat independent of systemic blood pressure (BP), the author suggesting a ‘mammalian diving response’ may be implicated, perhaps by raising cerebral perfusion pressure.
  3. Cavernomas and unruptured intracranial arterio-venous malformations (AVMs) trials (ARUBA) were presented, the clear take home message being avoid intervention in unruptured AVMs and cavernomas. Conservative management yielded a risk reduction of 73% vs. intervention in unruptured AVM management,6 probably the largest treatment effect (or non treatment effect) ever seen in stroke!

Other topics which came up frequently were cerebral amyloid angiopathy (CAA) and, closely related to this, cerebral microbleeds (CMBs). The expanding clinical spectrum of CAA led the Boston group to look at the different pathological, genetic and imaging phenotypes of CAA with ICH and CAA without ICH. The CAA with ICH phenotypes showed increased cortical superficial siderosis (cSS) in particular disseminated cSS and increased levels of apolipoprotein epsilon 2, whilst non ICH CAA phenotypes were associated with apolipoprotein epsilon 4. Interestingly both groups had similar “vasculopathic changes” (changes associated with ICH) in their blood vessels suggesting there are other pathological changes associated with ICH risk that are yet to be discovered.

The effect of CMBs on stroke risk in a population based cohort (Rotterdam study) was presented. Subjects with CMBs in a strictly lobar distribution (suggestive of CAA) were found to have a 5.25 times risk of ICH compared to those without CMBs, but did not carry an increased risk of IS, whilst those subjects with CMBs in a non lobar distribution were found to be at risk of both ICH (OR 5.77) and IS (2.6). Lastly a meta-analysis was presented revealing CMBs increased the risk of spontaneous ICH by roughly two in thrombolysis, however clinical outcomes were not examined so this should be considered hypothesis generating only.

Stroke is an exciting field with excellent research opportunities for both neurology trainees and medical trainees. Next years meeting is in Barcelona, Spain and I would strongly suggest you attend.


  1. Goyal M, Demchuk AM, Menon BK, Eesa M, Rempel JL, Thornton J, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. The New England journal of medicine. 2015;372(11):1019-30.
  2. Jovin TG, Chamorro A, Cobo E, de Miquel MA, Molina CA, Rovira A, et al. Thrombectomy within 8 Hours after Symptom Onset in Ischemic Stroke. The New England journal of medicine. 2015.
  3. Ruff CT, Giugliano RP, Braunwald E, Hoffman EB, Deenadayalu N, Ezekowitz MD, et al. Comparison of the efficacy and safety of new oral anticoagulants with warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials. Lancet. 2014;383(9921):955-62.
  4. Graham DJ, Reichman ME, Wernecke M, Zhang R, Southworth MR, Levenson M, et al. Cardiovascular, bleeding, and mortality risks in elderly Medicare patients treated with dabigatran or warfarin for nonvalvular atrial fibrillation. Circulation. 2015;131(2):157-64.
  5. Kuramatsu JB, Gerner ST, Schellinger PD, Glahn J, Endres M, Sobesky J, et al. Anticoagulant reversal, blood pressure levels, and anticoagulant resumption in patients with anticoagulation-related intracerebral hemorrhage. JAMA : the journal of the American Medical Association. 2015;313(8):824-36.
  6. Mohr JP, Parides MK, Stapf C, Moquete E, Moy CS, Overbey JR, et al. Medical management with or without interventional therapy for unruptured brain arteriovenous malformations (ARUBA): a multicentre, non-blinded, randomised trial. Lancet. 2014;383(9917):614-21.

To cite: ACNR 2015;15(4):25