CT versus LP – dawn of the thunderclap headache

As for dogmas to be lysed, no falsity is more resilient than the one that every thunderclap headache (TCH) needs to be tapped to rule out subarachnoid hemorrhage.

Walking through the numbers, our 90,000 pt emergency room probably treats 2,000 headache patients yearly, with 5-10% being thunderclaps, i.e. about 100-200 patients – let’s assume 200. We know from old (Landtbloom 2002) and new (Sayers 2015) series that about 7-15%% of these will be real subarachnoids or about 30 bleeds a year in the worst case. If we tap all of them, we will necessarily induce 10-20% = 40 artificial bleeds, which – according to the best literature we have – is at least hard if not impossible to differentiate from real bleeds:

  •  the red blood cell (RBC) count need not decrease in artificial bleeds
  •  but it can in SAH
  •  Xanthochromia, Ferritin, erythro- and siderophages need time to develop
  • there is no proper threshold for RBCs.

If you look at Sayers 2015 series of LPs in TCH, about 15% were uninterpretable and 13% were inconclusive, while 4% were clearly positive. This amounts to 32% LPs that lead to further workup or 64 patients a year for us. Of these 64 patients between 2% (if you use CTA) or up to 5% (if using DSA) harbour incidental harmless aneurysms, so about 2 patients will have one, which then is coiled or operated on.

On the other hand, at most 1 patient of our 40 real subarachnoids yearly will be CT negative (regardless of the time – see Sayers or Dubosh 2016, but at least in the first 6-24 hours). Unfortunately our LP workup for SAH in Germany (visual inspection for xanthochromia) only has about a third sensitivity. We don’t really know how many SAH do have enough red blood cells in their lumbal CSF and what a proper threshold might be. So it turns out, that we might actually miss the one CT negative patient after all.

In all this discussion I did not even consider other adverse events of lumbar puncture.

Here, then, is my take on the issue:

  •  TCH is way more complex than just ruling out SAHs. Think about the differential (see below) and do a proper history, physical exam and ensure follow-up, if possible with MRI (think of RCVS, SVT and other stuff). A rate of two thirds etiologically unresolved TCHs („primary“) is too much.
  • Always keep in mind that Hunt and Hess I-II may actually have a better prognosis than H&H III-V.
  • Discuss the probabilities with your department and your patient and be reasonable: LP is not the goldstandard test for subarachnoid!
  • If you do an LP to rule out SAH, leave at least 12 hours time (from onset) for xanthrochromia to develop and yes: all this time the patient is in danger, but the probability that he has an SAH is extremely low.



Hemicrania continua

Since on our ward we are dealing with strokes mainly, there is a tendency to forget basic neurologic knowledge, in particular in emergency settings. This happened recently in the following case: a 43 yo storage worker comes at 2 am into the ER, complaining about 4 months of unilateral headache, non side-shifting, with ugly exacerbations from his usual 4 to 8-9/10. Upon examination you discover a Horner syndrome and some tearing and noserunning. Interestingly he describes unilateral photophobia.

This is not a dissection, neither an SAH. As with all headaches history is the way to get to the truth, and maybe some treatment. Here are some important questions to ask:

  • Does the headache shift side?
  • Is it diurnally fixed?
  • Worse on lying than on standing?
  • Better with rest?
  • Loccally triggerable?
  • Visual disturbance?
  • Nausea/vomiting?
  • Photo-/phono-/osmo-/kinetophobia? Unilateral?
  • What triggers are there?
  • What drugs help? 

In all the trigeminoautonomic cephalagias, you have to get a picture (i.e. MRI)  eventually, but this should not preclude from treatment. Try oxygen 100%, triptans and indomethacin. Our case does have hemicrania continua, which by definition should react to this unique drug – but this is recently doubted.

References: in addition to the above article try the series of Peter Goadsby’s lectures on headache on YouTube.

Cluster headache and the wonders of oxygen

Your patient is not so young anymore and female. Her headache is not perfectly Cluster (now continuous for 3 days), yet it started out fairly typical. Then someone comes by, insufflates some oxygen, she gets better and bang – it has to be Cluster.

Even if you don’t believe in the all primary headaches are spreading depression slogan, you would be surprised if success of oxygen therapy were specific for Cluster headache. Here is a paper that shows some benefit for all primary headaches in an ER.

In today’s session we review Cluster headache and the other trigeminovascular headaches I know (not too many), using

Remember there are some ophthalmologic differentials for cluster:

  • orbital infection/imflammation
  • glaucoma
  • scleritis
  • uveitis.


Hypertrophic pachymeningitis

An MRI with thick dura and lots of contrast enhancement all around the head – this is the opening to a broad differential. Generally speaking, you have to differentiate between low pressure and inflammatory changes – so a spinal tap helps a lot and should be done soon. If inflammatory you face on of the various secondary causes of hypertrophic pachymeningitis or the idiopathic form (as in our case). There is good german article on the subject from 2006 and not much has been published on the subject apart from case reports.

For locals: in my folder there is a ppt presentation of a case of granulomatous idiopathic hypertrophic pachymeningitis…