Which side is affected in lateral canal BPPV?

From the rate of vertigo talks you can probably infer that either I must be very interested In or very insecure with vertigo. In fact, both is true.

So here is today’s problem: assume we know how to recognize horizontal canal BPPV and how to differentiate it from the other forms. Then there is still the difficulty in determining the affected side, because often enough it is not evident at all (this is not just my experience).

More concretely, we have a 56 yo saleswoman that wome up with extremely disabling vertigo. The world started spinning (horizontally, she says) when she turned over in bed to her alarm clock and she is not able to move since then, vomiting profusely on the slighest head turn. We managed to throw her around through our basic screening maneuvers – Dix-Hallpike and head-roll-test (also known as Paganini-McLure), where she showed purely horizontal decrescendo nystagmus towards the underlying ear on turning to either side – this is geotropic nystagmus. There is slightly more vertigo on turning to the left äs compared to right, but the nystagmus is pretty much the same.

Many maneuvers have been proposed for this situation and there is even some basic data about test theoretic properties of some of them. From this evidence I suggest the following successive tests (which actually can be performed during the screening phase).

  • History: which side is worse to turn to when supine? About 56% of patients can determine that and they usually are right.
  • Pseudospontaneous nystagmus: 56,2% have a spontaneous nystagmus when sitting straight, which – in the canalolithiasis situation – will abate eventually and is due to the purported angle of about 20-30° the lateral canal has wrt the horizontal plane (frontal arm is higher up than the other).
  • Lying down = supine nystagmus: in the so called Asprella diagnostic maneuver (which I love as a screening method for positional vertigo) you just move your patient quickly to the supine position, holding the head straight and record eye movements. In most of positional vertigos some nystagmus will come up and depending on the form of nystagmus you perform other maneuvers. Well, in this position about 75% (!) of lateral canal BPPV patients have some nystagmus and you can use the direction of nystagmus to determine the affected side (see table below).
  • Nystagmus intensity during the head-roll-test: due to some of Ewald’s laws (in fact, the second), nystagmus should be worse on the affected side in canalolithiasis. This happens to be the case in about 81% in the above mentioned article.
  • Bow-and-lean-test: when you bow the head of the sitting patient over the 30° angle the affected lateral canal has wrt the horizontal plane you should be able to evoke a the bow- or bending-nystagmus in about 59%. When leaning back a similar nystagmus can be observed (this is actually the pseudospontaneous nystagmus mentioned above). Both happens in only 40%.
  • Head-shaking nystagmus: any proper vertigo workup should include the screening for head shaking effects. The nystagmus evoked can be due to several reasons, but in lateral canal BPPV it produces a nystagmus in 62,5%.

Performing all of these maneuvers and then integrating the results with the table below, you should get the affected side right most of the time. Yet, if your treatment maneuver is then not effective, you should try the other side at least once, before starting a workup for other etiologies (central positional vertigo) as well.

 

Geotropic

R

L

Apogeotropic

R

L

Vertigo worse when supine
and turning to

the affected side

R

L

the unaffected side

L

R

Pseudospontaneous nystagmus towards

the unaffected side

L

R

the affected side

R

L

Lying down (supine) nystagmus towards

the unaffected side

L

R

the affected side

R

L

Nystagmus worse during head roll test towards

the affected side

R

L

the unaffected side

L

R

Bowing nystagmus
towards

the affected side

R

L

the unaffected side

L

R

Leaning nystagmus
towards

the unaffected side

L

R

the affected side

R

L

Head shaking nystagmus towards

the unaffected side

L

R

the affected side

R

L

Bloody tap? Postoperative shunt infection? How to do a CSF erythrocyte correction…

So it must have been a bloody tap the last time when we got an inflammatory CSF with 375 WBC/µl out of this guy on our ICU. A week later we come back to check on the cell count and it comes red. Not just one glass but all of them. Is the infection gone then?

We run through the arithmetic, using the standard formula for the cell index

WBC [CSF] / WBC [blood]
——————————–
RBC [CSF] / RBC [blood]

Obviously the ratio of cells in the CSF and blood should be the same unless there is some autochthonic cell “production” – this is quite similar to Reiber’s ratios for quantitative immunoglobulin production.

A value of the index of > 5,2 or a rise by more than 4 is purported to be specific for local infection.

Sources? Hard to say. This is probably neurosurgical folklore. I did not find a proper reference for it, but there is some data by  Schmutzhard of eVD patients to support it.

Fahr’s disease

After stumbling over a CT of a slightly parkinsonian woman with typical calcifications, I tried to read up on Fahr’s disease aka striopallidodentate calcinosis. Tried – i.e., unsuccessfully. Here is an article about it. And here is a review, which I cannot download. I did not find a proper entry in my standard textbooks the goes further than to add it to the list of metabolic symptomatic Parkinson syndromes. There are a lot of case reports along the lines “We saw it and then we read up on it”, but nothing really systematic.

Here are the highlights:

  • Require calcifications in the dentate nucleus and the basal ganglia, possibly more.
  • Expect Parkinsonism and ataxia, possibly more.
  • There is a connection to Ca metabolism disorders, in particular hypoparathyroidism and pseudohypothyroidism, possibly also due to the treatment of these disorders.
  • Guess what: there are familial and sporadic forms.
  • Guess what: no proper treatment.

Non-organic paresis and the Hoover sign

About 16 years ago, a patient had a spinal tap in our house and was discharged – we don’t know much about the details. After the deed she developed a hemiparese with hemianopsia and sensory disturbance, which led to an extensive workup in a university hospital and half a year of rehab.  Thereafter the patient was discharged in a wheelchair, then 33 years old. Since, she managed to work herself out of her wheelchair and – with the help of the pope – to walk again, still with a Wernicke man walk. In the meantime she seems to have been treated for bipolar disease, although again we don’t know much about the details. She is now on our ward for suspected basilar embolus and shows a highly suspicious hemiparesis without any Babinski or reflex difference.

We discuss some aspects of the clinical examination of hysterical paresis, focussing on the physiological coinnervations and particularly on Hoover’s sign, which we demonstrated in the patient.

As for functional / medically unexplained / non-organic symptoms in Neurology, there is a lot to think and talk about. I find the practical “british” approach of Stone’s school very attractive, so I highly recommend this article about diagnosis, it’s companion article about management of functional symptoms and the rest of Jon Stone’s articles in the JNNP and elsewhere.