European Stroke Organisation Conference (ESOC)
May 16–18, 2017

May 17, 2017
What if I told you that nearly 1/4 of ischaemic strokes weren’t caused by emboli at all? With the focus on retrieving clots with clever devices, and preventing them from forming with anticoagulants, it’s easy to forget that some ischeamic strokes have quite a different cause.  Lacunar strokes are caused by small vessel disease: an intrinsic disease of the small deep perforating arteries. Small vessel disease also causes vascular dementia, and is likely to  play a role in gait disturbance and falls.

At ESOC, there was an excellent session on SVD, which gave plenty of practical advice and food for thought.

We started with an update on imaging by Eric Jouvent. As SVD can be either sporadic or genetic, we often ask the radiologist if he or she thinks the patient may have genetic SVD. Whilst there are some signs to point you towards a genetic cause, these is no specific way of excluding one.  So, it’s back to a clinical suspicion, history, and examination.

Maco During then summarized the recent evidence for blood brain barrier involvement, drawing closingly on slides from Joanna Wardlaw, who was not able to be present. There’s increasing evidence to point to disruption of the blood brain barrier as a key cause. However, imaging in directly in vivo is difficult, though much work has  been done with DCE-MRI. The DCE MRI findings vary with age, with a more prominent association in older age, perhaps suggesting that the BBB damage may be a late feature of SVD.  Other advanced imaging features included measures of water diffusion (mean diffusivity) with diffusion imaging being able to capture the damage at an early stage.

Hugh Markus summarized the limited evidence on SVD treatment available now. There has been one good quality study, the secondary prevention of small subcortical strokes (SPS3) study from Canada. The rest of the evidence comes from trials that included all subtypes of stroke, including lacunar stroke, and didn’t differentiate the stroke subtypes very well. There is evidence that anticoagulants are harmful, except in patients with atrial fibrillation, and that single agent antiplatelets are probably beneficial. Blood pressure lowering to 130 systolic is probably effective, but there is limited evidence to lower any further. Thrombolysis appears to be effective.

In the future, more trials are needed to find effective treatments for lacunar stroke: The PRESERVE trial is currently investigating management of blood pressure. It’s also worth mentioning the LACI1 trial, which is about to go nationwide from Edinburgh, and is investigating the role of isosorbide mononiratie and cilostazol.

It’s good to know that the excitement about thrombectomy hasn’t stopped people from researching lacunar stroke.

Please note the following conflict of interest: Joanna Wardlaw was my PhD supervisor, and I have contributed towards some of the work presented at this session.

—Stephen Makin, PhD