Vascular Neurology
13 cases on acute ischemic stroke thrombolysis and thrombectomy, secondary prevention, anticoagulation timing, and intracerebral/subarachnoid hemorrhage management — choose a case below to open its full multi-voice debate.
A stroke alert inside the standard treatment window, with two guideline-acceptable fibrinolytics on the shelf and no stated preference between them — the disagreement is about which one, and about a dosing mix-up risk neither drug's own trial data addresses.
Perfusion imaging can make a strong case for treating a stroke of unknown onset time — but the newest trial testing that logic with tenecteplase specifically, rather than alteplase, didn't confirm it, and the case for extending the newer drug's own use into this window is weaker than it looks at first read.
A patient's pressure stays elevated after a clean thrombolytic run, and the instinct to keep pushing it down runs straight into a large trial that found intensive lowering did prevent bleeds — without improving a single point of function.
Hyperglycemia after a stroke looks like an obviously fixable problem — until the trial built to fix it found nothing to show for the effort except more dangerously low blood sugars, and the team has to decide how tightly to actually control a number that looked worth controlling.
A high-risk TIA is exactly the population two major trials built the case for short-course dual antiplatelet therapy around — the disagreement isn't whether to start it, but how long a habit borrowed from cardiology practice should be allowed to run before the bleeding risk catches up with the benefit.
Two patients, both newly diagnosed with atrial fibrillation after an ischemic stroke, land on opposite ends of a real trial's own confidence range — one whose infarct size argues for real caution even under the newest evidence, one whose imaging clears every bar for starting early.
High-intensity statin for everyone with a recent stroke is the reflexive answer — but the trial built specifically around this stroke subtype found benefit from hitting a target, not from maximizing a dose, and the difference matters for a patient whose LDL is already most of the way there.
A stroke that looks embolic but has no confirmed source tempts the reflex to anticoagulate against a hidden cause — three separate randomized trials, including one that specifically pre-selected for the biomarker profile this patient carries, have now tested that reflex and found nothing to show for it.
The one agent built specifically to reverse this bleed carried the only randomized data showing it also raises the recipient's own risk of a new clot — in the very organ everyone is trying to save. That finding is why it is no longer sold in the United States, and why tonight's decision is about what is left on the shelf.
A clopidogrel prodrug that never gets activated protects nobody — a genetic test can catch that in advance, but only if the result comes back before the decision has to be made, and the alternative of treating everyone with the stronger drug carries its own real cost.
Two major trials tested the same aggressive blood pressure target in intracerebral hemorrhage and reached different-flavored answers, and a third that finally showed a real benefit did it by testing a whole bundle of interventions at once — leaving genuinely open how much of that benefit belongs to the pressure number itself.
An entire generation of drugs has reduced angiographic vasospasm without ever improving how the patient actually does — a striking, repeated pattern that leaves nimodipine standing alone, and raises the harder question of what a genuinely refractory case should reach for when the one proven drug isn't enough.
The trial built to compare two long-term antiplatelet regimens head to head failed to establish either as noninferior to the other — so the real decision, months out from the stroke that put this patient here, comes down to bleeding, tolerability, and which regimen she will actually keep taking.