Session Report: Stroke Beyond the Brain: Systemic and Hematologic Drivers of Cerebrovascular Events

The teaching course “Stroke Beyond the Brain: Systemic and Hematologic Drivers of Cerebrovascular Events” showed how often stroke reflects a systemic, hematologic, or immune-mediated disorder rather than an isolated cerebrovascular event. Chaired by Xabier Urra (Barcelona, Spain) and Natalia Perez de la Ossa (Badalona, Spain), the session brought together clinically relevant perspectives on thrombophilia, vasculitis, antiphospholipid syndrome, and thrombotic microangiopathy.

The speaker pointed out a strong reminder that precision stroke medicine often begins with recognizing systemic red flags. The most consistent themes across the course were broad differential diagnosis, thoughtful laboratory testing, and urgent multidisciplinary treatment when APS, vasculitis, or TMA/TTP is suspected.

1.Hematologic disease and hypercoagulability

Annette Fromm (Bergen, Norway) provided a concise overview of hematologic disorders associated with prothrombotic states and hyperviscosity, emphasizing that both mechanisms often overlap in clinical practice. Particularly helpful was the structured review of inherited thrombophilia set against the broader background of venous thrombosis and possible arterial ischemic risk.

She summarized that acquired hematologic conditions such as sickle cell disease, cancer, myeloproliferative disorders, and multiple myeloma also contribute substantially to stroke risk. The talk made clear that these risks are usually shaped by a combination of patient-related, disease-related, and therapy-related factors.

2.Autoimmune disease and stroke

Hubert de Boysson (Caen, France) framed systemic vasculitis as an important diagnostic model for stroke medicine, spanning small-, medium-, and large-vessel vasculitides. One of the most practical aspects was the focus on work-up and disease activity. A strong point was the recognition that autoimmune stroke mechanisms are often mixed rather than isolated, with inflammatory disease coexisting with atherosclerosis or small-vessel disease. Clinical examples such as anterior ischemic optic neuropathy and ANCA-associated vasculitis illustrated how careful phenotyping remains essential.

3.Antiphospholipid syndrome

David Werring (London, United Kingdom) highlighted the clinical complexity of antiphospholipid syndrome (APS) in patients with ischemic stroke and TIA. APS appears to be particularly relevant in younger patients with cryptogenic stroke, although the relationship between antiphospholipid antibodies and ischemic stroke remains difficult to quantify because antibody findings may be transient or not clearly causal.

A major practical highlight was the discussion of who should be tested: younger adults with unexplained ischemic stroke, patients with prior venous thrombosis, pregnancy-related stroke or pregnancy loss, and those with hematologic abnormalities such as thrombocytopenia or anemia. Equally important was the caution that acute-phase testing can be misleading, making repeat confirmation after 12 weeks essential in many cases.

The most debated part of the lecture concerned treatment. Evidence for antithrombotic management remains limited and practice varies considerably. The session finally underscored the need for rapid recognition of catastrophic APS and for multidisciplinary management in refractory cases.

4. Thrombotic microangiopathy

Arthur Liesz (Munich, Germany) presented thrombotic microangiopathy (TMA) as an important and time-critical stroke differential diagnosis. A central take-home message was that frequent CNS involvement means stroke physicians should think of TTP early when neurologic symptoms occur in the setting of thrombocytopenia and hemolysis.

The diagnostic part of the talk was especially practical, with emphasis on ADAMTS13 testing, the PLASMIC score, and the need to start plasma exchange as early as possible. The treatment section highlighted how outcomes in acquired TTP have improved markedly with plasma exchange, corticosteroids, rituximab, and caplacizumab, while complement-mediated TMA has opened an additional therapeutic perspective with eculizumab.