Socrates and Sophistry

The Death of Socrates

Socrates, the Classical Greek Philosopher (469 BCE – 399 BCE), was the forefather of questioning dogma. Through the writings of Plato, we understand that Socrates believed in dissecting and deconstructing firmly held beliefs and convictions. He famously invited any members of public to debate with him (including women!!), in order to distil out truth where there appeared to be none. He would start an argument from the position of believing one knew nothing, instead of the other way around. He is famous for his quote: ‘I am the wisest man alive, for I know one thing, and that is that I know nothing’

We could do with a bit of Socratic thinking once in a while in medicine.  So much dogma, and well-worn explanations get handed down from textbook to teacher. And they are not always right.  Or believable.

The Socrates and Sophistry section promises many questions. And just maybe, with the input of the many and varied smart LITFL blog readers, possibly answers.  At least we may be able to debunk some of the pat clichés which we have been offered as the explanations for some of the medical conundrums we come up against. Some of these questions may not have answers at all, but better to admit that some things are unknown, rather than the query being patronizingly patted on the head with misinformation.

So without further to-do… let us begin with the first of the Socrates and Sophistry series, LITFL style – by putting out to the readers our first question. Are we dealing with myth or medicine, dogma or doggy doo, science or sophistry?

Question:

What causes T wave inversion on the ECG in the setting of some subarachnoid haemorrhages?

Because the sympathetic storm induced causes subendocardial myocardial ischaemia.

Why do we not then see a similar pattern in other circumstances causing sympathetic stress, or other similar cerebral pathologies?

Feel free to submit ANY answer to the comments section – we would love to hear your own thoughts, first principle analysis, expert exegesis or revel in revered references.  Remember NO answer can be wrong…otherwise we’d know the right answer already! If you want to discuss ‘Socrates and Sophistry’ topics on Twitter, use the #LITFLSAS hash tag.

If you have your own question, please submit it to… Michelle @ lifeinthefastlane.com

Print Friendly

Comments

  1. Duncan says

    I doubt the answer is as simple as that explanation, but in it’s defence I have seen pseudoinfarction ECGs in ischaemic CVA and amphetamine toxicity , and Tako-Tsubo cardiomyopathy is well documented. These all support parts of the sympathetic storm theory (or at least a common process with all of these pathologies affecting the ECG), as does the frequency of neurogenic pulmonary oedema. Going against it somewhat are the fact that the (transient) ECG changes I have seen with ischaemic CVA did not seem to have any other evidence of sympathetic crisis (e.g. diaphoresis, tachycardia) although hypertension is obviously pretty common.

    • says

      I agree Duncan -- there seems to be examples both supporting and refuting the sympathetic storm process. I didn’t particularly want to weigh into the debate at this point, as I am far fuller of questions rather than answers, but in my polling of neurosurgeons in a quaternary subarachnoid service in Florida, there seems to be some support that there are individuals who have a genetic predisposition to this sort of subendocardial ischaemia in stressful events, which may then support why we see Takotsubos in only a certain population. Still doesn’t quite bridge the logic gap though.

      • says

        Great topic but a tricky one as there is little in the way of good evidence. I’d always gone along with the sympathetic surge concept. This article (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077842/?tool=pubmed) suggests “hypothalamic stimulation as well as autonomic dysregulations have been implicated as causative for the ECG changes in SAH without corroborative conclusive evidence”. It’s been described since 1947 and other explanations last century have included hypokalaemia, stimulation of area 13 under the frontal lobes, hypertension, increased parasympathetic drive as well as increased sympathetic drive, which seems to have the most indirect evidence to back it up. Against this theory is a paper that showed no difference in urinary catecholamines between a group of SAH pts with ECG changes vrs a group that didn’t, but there were problems with the study, although a bigger and better study did show a correlation (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC458883/?page=1) and this is about as good as the evidence gets! Why doesn’t is happen in other catecholamine surge states? Not sure, maybe it does. After seizures it can happen and can also lead to Takotsubo’s; be keen to hear more thought son this one.

  2. Minh Le Cong says

    Does the question require an answer?
    One theory You have made me mull over during one of my long retrieval flights is that some people with SAH will have CAD to a degree. Not everyone with CAD has ACS or ECG changes. When you have your SAH the catecholamine surge will more likely cause ECG changes in those with CAD with significant stenosis..sought of like a dobutamine stress ECG test if you will,
    same goes for other hypersympathetic, catecholamine excess states.
    In other words the SAH does not cause the cardiac ischaemia per se, it promotes the state whereby ACS and ECG changes will occur in those with CAD…it is a form of provocative cardiac testing.

    • says

      We were definitely after mulling. Excellent and innovative thoughts Minh. Hopefully soon we will collate some of the brilliance from here, and twitter, with a smattering of expert opinion, to see what a collective postulate might look like.

    • says

      Minh,
      That has been described for trop rises and so forth in ischemic CVAs, but the underlying cardiac disease hypothesis doesn’t bear out in the SAH studies I’ve looked at.
      Check out the #LITFLSAS hash tag on twitter for the discussion and references.
      Chris

  3. Joe says

    I agree with Minh’s theory. The catecholamine surge after aSAH rupture sets of a cascade of events stimulates a sympathetic storm. It would be safe to say that those with preexisting cardiac disease are at higher risk for cardiac dysfunction post aSAH. So which came first the chicken or the egg?

    Also the standard therapy for SAH may also exacerbate the risk to cardiac muscle by decreasing coronary perfusion pressure.

    This article http://www.ncbi.nlm.nih.gov/pubmed/11248297 asserts it’s rare to find actual CAD in SAH patients.

    Another article http://www.ncbi.nlm.nih.gov/pubmed/16267258 suggests poorer outcome in SAH patients with elevated troponin.

    Certainly a lot more questions than answers.

  4. says

    I agree that “sympathetic storm” is a facile explanation since it fails to either capture the entirety of what we see in those situations, nor explains why it’s absent in other overwhelmingly sympathetic states. (It also tends to deteriorate into handwaving or hurriedly clicking to the next slide before anyone asks what on earth you’re actually referring to.) At the same time, I think the common elements we see between intracranial insults, Takotsubo, vasospasm, etc. cannot be ignored.

    With all of that said, we could also ask whether it matters beyond the academic question. Would understanding the exact etiology be helpful? I suppose it might suggest a targeted way to treat it, but I haven’t seen many cases where the resulting clinical effects (HF etc.) are dire and not amenable to more generalized therapy.

    • says

      I agree with you Brandon, that it may not matter much beyond the academic question -- although surely then it would be better to admit that the answer is unknown, rather than the propagation of inaccuracy. And you never know, with the collective brilliance of the LITFL readers, as demonstrated thus far, maybe we can advance the understanding a bit further. If nothing else, the LITFLers all like a bit of intellectual gaming :-)
      We won’t know the therapeutic implications, or extrapolations until we understand it.

      With the fullness of time we’ll collate the responses and references, and see what we come up with.

      • says

        I do agree! In fact, I think this type of situation isn’t uncommon… we naturally ask “why?” when we encounter an unusual phenomenon, but if we instinctively feel the answer may not matter much, we tend to accept whatever pat response comes back without trying to unpack it, or even verify it. (“Vagal tone? Again? Well, okay then.”) Trying to break past that apathy barrier, even just to have a discussion like this but all the more so when, say, proposing new research, can be a challenge…

    • says

      If I remember correctly, Faraday’s discovery of electromagnetism was criticised for it’s lack of practical implications….
      The potential applications of new found knowledge are rarely predictable.
      Chris

  5. says

    We may not yet have a plausible and logical progression of causation yet, but we’ve certainly moved on from the pat explanation previously proffered. Thanks to @pbsherren @precordialthump, Oli Flower, Duncan, Minh, Joe and Brandon above, we are somewhat agreed upon:
    1) Subarachnoid blood is an irritant at meningeal level around the vasomotor centre
    2)There is likely to be some sustained catecholamine surge associated with this (although it may have a heterogeneous output)
    3) There are several ECG changes seen, not just the classic deep T wave inversion, but also ST changes, U waves and prolonged QT segments. Malignant arrythmias are also seen in this setting. All of these changes are related to abnormal repolarisation.

    HOWEVER: The T wave inversion seen in SAH is often persistent -- in the region of weeks -- thus it can’t be simply related to that initial catecholamine surge. It’s not clear if it associated with a predictable troponin rise, suggesting a NSTEMI, whatever the cause.
    Why do some patients, and not others, with equivalent grade of subarachnoid, manifest these ECG changes? What is the common pathophysiology with similar ECG appearances in other conditions? And why such DEEP T wave inversion, that frequently sets it apart on initial glance from other conditions, such as post STEMI/post takotsubos, other causes?
    Are we too focussed on the catecholamine surge being the link between the meningeal irritation and the depolarisation changes on the ECG? Could there be another middleman being the culprit entirely??
    The references quoted above are useful, plus the one mentioned in #LITFLSAS -- http://www.ncbi.nlm.nih.gov/pubmed/1501769

    So -- just an interim summary really -- the feelers continue to be put out round the globe.

    We’ll only close off the discussion when we can happily say logic is the winner.

  6. Andy Chapman says

    Not sure if this adds much to the already proferred wisdom but this little article ( Cleve Clin J Med. 2008 Mar;75 Suppl 2:S26-30.), suggests a potential inflammatory model in conjunction with the classic catecholamine surge. Makes more sense to me given duration of changes and frequent appearance in patients who clearly don’t have CAD (seen it in several girls in their twenties).

Comments