I'm interetsed to find out if tnk works at all in lacunar strokes or (small-ish) strokes that have no salvageable penumbra, at all, regardless of the severity. (it's 2026, MRI exists now)
You can have a tiny <1 mm artery occlude and get a disabling lacunar stroke. how is tnk going to lyse that tiny vessel open, it's all calcium, atherosclerosis, lipohyalinosis in there.
And conversely, perhaps the reason tnk fails with minor stroke is precisely because most minor strokes are little, there's nothing to lyse..
PS
check out the tenCRAOS trial in the nejm, if you haven't already.
I don't have the insight into what the "penumbra" looks like in the microcirculation surrounding a lacunar injury, as opposed to the rough approximations of collateral circulation and time delay created by CTP. In such a small space, is micronutrient flow and diffusion stronger? Is it more/less/similarly protective? Or, are lacunes just quick 15-minute infarcts with minimal response? Our understanding of the underlying process being treated (including clot length/composition) in the acute setting is so minimal (yay non-con CT in the stroke bus), we're basically just cavemen hitting ourselves on the head with a hammer.
Ah, well, I'm sure I can be incriminated by selective citation as well – one could argue I've discarded all manner of observational evidence regarding the ongoing "disability" of patients with "minor stroke" (as you say, the definitions are amorphous).
The real key is, at least in the U.S., this is all sort of hand-waving – no one wants to be on the hook for a lawsuit if a seemingly "non-disabling" stroke ultimately results in long-term annoyance. Add that to the bias towards action and the idea IVT is harmless in stroke mimics, and the IVT will flow ....
I'm interetsed to find out if tnk works at all in lacunar strokes or (small-ish) strokes that have no salvageable penumbra, at all, regardless of the severity. (it's 2026, MRI exists now)
You can have a tiny <1 mm artery occlude and get a disabling lacunar stroke. how is tnk going to lyse that tiny vessel open, it's all calcium, atherosclerosis, lipohyalinosis in there.
And conversely, perhaps the reason tnk fails with minor stroke is precisely because most minor strokes are little, there's nothing to lyse..
PS
check out the tenCRAOS trial in the nejm, if you haven't already.
I don't have the insight into what the "penumbra" looks like in the microcirculation surrounding a lacunar injury, as opposed to the rough approximations of collateral circulation and time delay created by CTP. In such a small space, is micronutrient flow and diffusion stronger? Is it more/less/similarly protective? Or, are lacunes just quick 15-minute infarcts with minimal response? Our understanding of the underlying process being treated (including clot length/composition) in the acute setting is so minimal (yay non-con CT in the stroke bus), we're basically just cavemen hitting ourselves on the head with a hammer.
Ah, well, I'm sure I can be incriminated by selective citation as well – one could argue I've discarded all manner of observational evidence regarding the ongoing "disability" of patients with "minor stroke" (as you say, the definitions are amorphous).
The real key is, at least in the U.S., this is all sort of hand-waving – no one wants to be on the hook for a lawsuit if a seemingly "non-disabling" stroke ultimately results in long-term annoyance. Add that to the bias towards action and the idea IVT is harmless in stroke mimics, and the IVT will flow ....