Localization of paralysis in stroke

What do you need to know about the paralysis of your patient to shorten the list of possible stroke locations?

  • Is the paralysis proportionately affecting arm and leg (brachiocrural) or more brachially or crurally or even a monoparesis?
  • Does it affect proximal or distal muscles or both?
  • How much and in what form is the face affected? Is the face afflicted during volontary and/or emotional innervation?
  • Is it purely motor? Is an associated sensory disturbance ipsi- or contralateral? Dissociated?
  • What cranial nerves are involved?

We discuss the anatomy of the corticospinal and corticobulbar (in particular the corticofacial) tracts, moving through the various levels

  • Cortical: primary motor cortex, sensory cortex, premotor cortex
  • Subcortical
  • Internal capsule
  • Cerebral peduncle
  • Pons
  • Medulla

We spend some time on the anatomy of the internal capsule – here, the centuries-old descriptions have been reconfirmed in tractography studies.

Some pearls

  • Monoparesis is rarely if ever capsular or subcapsular.
  • Pure motor proportionate paralysis tends to be capsular.

As for references, I highly recommend Brazis’ Localization book (the first chapter), complemented by the recently edited Stroke Syndromes book (aka the bible).

Acute management of anticoagulation-related intracerebral hemorrhage

You rush to the CT with your latest thrombolysis candidate that might not have taken his oral anticoagulant, fearing the INR results that might necessitate endovascular therapy rather then thrombolysis, when, alas, you find the ICH. You exhale slowly and then think about what to do next. Here is what I recommend for the first 2 hours

  • Lower the pressure (which nearly always is raised) with your favorite iv antihypertensive to at most 140/90 mmHg
  • Consider CTA to find the spot sign or even some pathological vessels
  • Call your favorite neurosurgeon (this is SOP in our house) to discuss surgical options
  • Reverse anticoagulation as quickly as possible, aiming (for the most prevalent case of Warfarin/Marcumar-associated ICH) for a Quick of 100% (expect 1-1,5% increase for every IU*kg, so the formula (100% – quick) / 1,3 * kg with a max dose of 5000 IE is a reasonable heuristic); add 10 mg of Vitamin K for good measure to ensure sustained INR normalization.
  • Establish proper blood pressure monitoring, usually with an arterial line
  • Check coags 30 mins after correction
  • Monitor clinically and by CT until you are sure that the bleeding has stopped
  • Expect rebleeding for at least 1 day


I can add another funny stroke mimic to the list of diagnoses that have been thrombolysed: heatstroke. We review what there is to learn about this old and modern disease. Here are some reminders:

  • The classic form (toddlers, elderly, nursing home residents, sick people) stems from exhaustion of the sweating mechanism, so the skin is dry while the temperature is up.
  • The exertional variant (marathon runners etc.) keeps sweating as much as it can, yet the heat produced is too much (and the behavioural compensation [stop running] is switched off by psychopathology and endorphins).

The latter case is an emergency medicine problem in the field. While it has some differentials, it is vital to

  • get a monitor
  • get a thermistor probe into the proper hole
  • cool as quick and as good as you can – preferentially a cold water tub. It seems that there is an age-old debate whether this is really the best option, because “theoretically” the body could shut down perfusion of the skin – I understand neither the physiology nor the physics of this caveat, so I’d recommend the tub anyway. The goal is to reduce core temperature to 39°C. Remember that the patient probably will not shiver (the thermostat still works).

The damage to the body stems from heat and it affects the brain, the liver, the kidney and the blood first, before destroying anything else. The longer and the higher the temperature is, the worse.

As for references

Induction, deduction and how experts think in medicine

The age old description of how science is (supposed to be) working to generate theories, refute them, induce statements from data and use the Popper/Pearson model to work on hypotheses does not apply to the non-scientific field of medicine. Since the seventies people have wondered how good doctors think and how to bring young ones to become good doctors. We discuss the various approaches to patients and their pathophysiology, to clinical data and thereby involve definitions of pattern matching, heuristics, induction, abduction and deduction as well as Bayes statistics to develop an understanding why working in medicine becomes more complicated and less efficient during the first years – what is known as the U-shaped learning curve of becoming a medical professional.

This is all but theoretical, but of course, you have to read the classic texts if you want to understand the details. Here is a short review on the main part of subject of today’s talk.

Brainstem anatomy, ocular tilt reaction and the subjective visual vertical

I found a few people that didn’t know the 4m4s-rule! So we did that once more. While declinating the various brainstem strokes we had on our ward today, we also spoke about the various ways that vestibular disturbances can be found, what the ocular tilt reaction is and how the subjective visual vertical works. To be honest, while I still marvel at the possibility to measure it with a simple bucket contraption (here is how they build them in Pittsburgh and here is how you can even throw your Iphone into the bucket), I find it exceedingly difficult to interpret the test – it should be less affected by peripheral than central disorders (with thresholds around 8-10°), but would you really forgo an MRI if the SVV is only 6° deviated?

BTW: A very short table exemplifying the “use” of the SVV is found in the wonderful article “A bucket of vestibular function”, written by the Brandt/Strupp/Dieterich clan.