It sounds rare and I have to admit that I have not seen it often – but probably it is often overlooked in the busy ER. So here is one of the secondary facial palsy types that you should be able to recognize: the patient reports some swelling in the face (usually the upper lip) at least in the past, more often concomitant with the facial palsy. Search for the combination

  • facial/lip swelling (recurrent)
  • cheilitis granulomatosis (probably from incomplete recuperation from the swelling attacks)
  • lingua plicata
  • facial palsy.
In diagnosed patients quite a lot of neurological symptoms are reported more often than expected. You can find a lot of detail in the respective chapter in a  thesis on facial palsy.

How to read the publication of a randomized controlled trial

Traditional evidence-based medicine a la Sackett has it that you should consider a couple of aspects about a randomized controlled trial, before you believe it. Using the chapter on RCTs in the User’s Guide and the SPARCL trial in the NEJM we discover quite a lot of flaws in this not quite so new trial, that spawned a lot of controversy about the bleeding complications of high dose statins – a topic on it’s own.

On my hidden agenda I wanted to also sharpen the minds about the disadvantages of large-scale RCTs. While I would not go as far as James Penston in his book or one of his articles to totally condemn them (hey, they are still the best – after n=1 trials – we’ve got in terms of research), it is worthwhile to understand why phase 3 RCTs are more an economic than a medical undertaking. So go on and read one of his articles, say this.

Quite curiously, we did not go into this topic as far as I would have wished and instead focused on p-values, confidence intervals and frequentist statistics – a topic we have to deal with again in the future (after I have read up on Fisher vs. Neyman-Pearson).


It is quite surprising that nearly every neurologist knows about porphyria and that it can present with psychosis and abdominal pain as well as neuropathy. The only problem is to do the right test to identify and do it quickly: morning urine sent for delta5-ALA, which probably is the offending agent in central and peripheral (including autonomic) neuropathy. We discuss a young female patient with a short psychotic episode after a presumed gastroenteritis and run through the core facts.

  • Abdominal pain or back pain in at least 80% of the patients – both being caused by autonomic neuropathy
  • Axonal predominantly motor neuropathy – one of the most important differentials for GBS, recognizable by neurophysiology
  • Hyponatremia can occur
  • All “neurological” porphyrias have delta5-ALA in the urine in the acute phase.
  • Skin lesions occur in varietage porphyria and hereditary coproporphyria.
  • Avoid drugs as listed on

Here is one good reference, taking only 4 pages.

Writing discharge letters

We are working on a concept for improving our discharge letters. This involves both structural and stylistic improvements. Here are the most important points:

  • The letter aims at the next care provider, the PCP mostly, but also the next hospital (including us if the patient is readmitted). It serves to convey the diagnosis (what?), a proof that the diagnosis is right, a very short description of the course (complications) of the treatment and a plan for future treatment. It should not serve as a notepad for daily events. It should not serve as a reminder for what to do on the next admission.
  • Give a good but not exhaustive list of diagnoses, citing only those that are relevant for the current admission.
  • Give a good and exhaustive history of current events.
  • Give a complete list of clinical and paraclinical results, erasing all unnecessary remarks (“the result was conveyed to the treating neurologist”).
  • Give 1-2 sentences that convey the diagnosis and a reason why it is correct.
  • If necessary, describe the course of the patient over 1-2 sentences, mentioning only important events.
  • Give a concise and exhaustive plan in bullets.

As for style I recommend this article.

  • Avoid redundancy at all cost.
  • Avoid set phrases such as “thanks for continuing the treatment”, “continue this treatment”.
  • Avoid “The past medical history is presumed.”
  • Avoid passive constructions, substantive constructions.
  • Avoid medical jargon, e.g. “An oral anticoagulation was initiated with Rivaroxaban.” – make it simpler: “We gave Rivaroxaban.”
  • … list could be continued

Sensitivity, specificity, predictive values, likelihood ratios – a journey through terminology using jolt accentuation

Since I am a mathematician I don’t easily scare, at least I am not scared by statistical terminology. Still, it is hard to remember the difference between

  • sensitivity, specificity
  • positive and negative predictive value
  • likelihood ratios

So I tried to find a good example to study these and came up with jolt accentuation for suspected bacterial meningitis. In short, jolt accentutation means (exacerbation of) headache upon 2/sec head turns and is purported to be more sensitive than neck stiffness by the first publication and by this JAMA evidence based medicine review. To get some real data, we used a tiny collection of Iranian patients and then started constructing the four-field-table.

Here is the grid:

True positive

False positive

Test positive

False negative

True negative

Test negative




And here are the formulas:

  • Sensitivity: TP / (TP + FN)
  • Specificity: TN / (FP + TN)
  • Positive predictive value: TP / (TP + FP)
  • Negative predictive value: TN / (FN + TN)
  • Positive likelihood ratio: TP / FP
    = sensitivity / (1 – specificity)
  • Negative likelihood ratio: FN / TN
    = specificity / (1 – sensitivity)

Want more?

  • You can use the likelihood ratios to calculate the posttest odds from the pretest odds: post odds = pre odds * likelihood ratio. Problem is: you need to use odds rather than probabilities and we usually don’t. Of course: odds = probability / (1 – probability) and conversely probability = odds / (1 + odds). If it’s too much of a hassle, use a calculator on your IPhone or use Fagan’s nomogram.
  • Likelihood ratios are independant of disease prevalence – all the info about the disease goes into the pretest probability.
  • Read up on these statistics in this wonderful short pdf.

The Closure trial – PFO and stroke

It took some time until the Closure data has been turned into a publication (this happend today). We review the evidence for PFOs vs. Stroke and then step into the muddy waters of interventional PFO closure, the critique of the study.

Here is my view on this:

  • PFO can be a cause of stroke. I truly believe it, when I get a good history of Valsalvas beforehand, find a DVT or – better (worse for the patient) – a pulmonary embolism, or even  a thrombus in situ. Otherwise I am hesitant to diagnose it, if any other cause is at least remotely possible.
  • PFO + ASA? I have never been convinced about thrombi being formed at this highly mobile atrial septum. Why shouldn’t it be even better if it is more mobile – scares of the thrombi…? So I don’t really share our german neurologic guidelines opinion that an ASA is worse and should lead to anticoagulation.
  • Therapy in PFO + stroke if reasonable causal relationship is proven? Our guidelines dictate anticoagulation if ASA is present, o/w ASS. Why not anticoagulate them all, assuming that a DVT must exist or at least have existed and thus a venous vessel wall injury persists? Then after half a year, switch to ASS.
  • PFO closure? Don’t. Unless… recurrent strokes on medical therapy, problems with anticoagulation, …