Using TCD for Valsalva

We use Valsalva’s maneuver at various places –

Although he was mainly concerned with bad ears, he somehow seems to have created a fold in the colon as well: Antonio Maria Valsalva (* 17. Juni 1666 in Imola; † 2. Februar 1723 in Bologna)
  1. to elicit certain cardiac murmurs (such as the one of HOCM)
  2. to slow down the heart rate for a diagnostic window in supraventricular tachycardia
  3. to quantify damage to the autonomic nervous system (as in small fibre neuropathy)
  4. to provoke a right-left-shunt in PFO testing

If you are not careful, you can even invoke Valsalva’s accidentally when you really want to determine cerebrovascular reserve.

In yesterday’s session we derived the four phases of the Valsalva reaction from the rudiments of what we should remember about cardiovascular physiology, in particular the baroreflex (carotid sinus), Bainbridge reflex and the role that the sympathetic and parasympathetic nervous system play as mediators of tachycardia/hypertension.

We then went on to examine the role of various practical parameters in the Valsalva maneuver, such as the depth of the initial inhalation, the length of straining (phase II) and the straining pressure, using transcranial doppler and an ecg to monitor the heart rate and blood pressure changes. In my experiences, TCD is still the best way to measure changes in blood pressure continuously if you don’t have an arterial line and cannot afford a Finapres device. But you have to make sure that you do not extend the straining phase too much (otherwise CO2 increases and you get an increase in flow), so I only use 10 seconds instead of the usual 15 seconds that are recommended (this publication seems to show that this is still ok).

We also discussed the inherent difficulties in defining normal values for autonomous nervous system examinations because of the wide variation in base vagal tone, reactivity, hydration and more.

References

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(Transverse) Myelitis

Diagnostic criteria for transverse myelitis

In our newly established CME series for residents we cover basic topics that every Neurologist should know. Today the topic is transverse myelitis, it’s acute management and imaging characteristics.

As for references we use

Reflex list – DTR only

I guess you can expect every mammal to know the basic reflexes, but it is quite hard to remember the list of advanced reflexes used in particular in peripheral neurology. So here is my list, just for reference. It does not contain the superficial reflexes (skin to muscle) or the pathologic reflexes. I remember doing a bit on the Babinski once.

List of all reflexes you can reasonably rememeber
List of all reflexes you can reasonably remember (in German only)

Classical gait disorders

It is an old saying that a Neurologist can only recognize those diseases that he can mimic. So we play around with various gait disorders, looking at youtube videos and trying to isolate the core examples.

More videos can be found here.

An update on thrombolysis

perfusion mapDespite the recent upheaval in the emergency medicine community about the ACEP tPA-for-stroke guidelines, thrombolysis is one of the two foundations of modern stroke medicine. In a local stroke symposium, I gave a talk about new developments and folklore in tpa-ology. It also exposes our Augsburg data on thrombolysis with bleeding rate and all you could wish in a real life tpa setting. The talk introduced a new acronym for remembering the various causes of tpa-related ICH (I love acronyms). It reads CORTEX

  • C erebral amyloid angiopathy (extraischemic ICH)
  • O ld stroke (old meaning > 6h)
  • R ecanalization (recanalized vessels to dead tissue)
  • T rauma (bleeding into contusions)
  • E ndocarditis (rare but sometimes fatal)
  • X – coagulation (think of factor X, anticoagulants, ASS and the like)

If you can read German, you might want to give the presentation a try – here is the prezi link.

Tullio, Hennebert and other absurd eponyms

If vertigo patients make you vomit, this post is nothing for you.

It is always exciting to watch medicine develop new concepts. While Neurology is certainly full of examples with new diseases, acro- and eponyms popping up everywhere, HEENT people seem to be more conservative, perhaps because they are busy operating and healing people. Superior canal dehiscence syndrome is a very young disease that  probably owes it’s discovery more to highres CT than to puzzled (neuro-)otologists. But now that we have learned how to deal with it, even the posterior canal can erode and be operated on, so perhaps a thorough neurootologic exam and neurophysiological investigations are in order when your patient tells weird stories (as SCDS-patients seem to do).

We discuss an example we pulled out of our ER recently which then went on to surgery and successfully had his superior canal plugged (not before a repeated workup in a specialized vertigo clinic) and who now is symptom free.

References

Tunnel vision and macular sparing

 I used to think psychogenic at once, then I added migraines to the differential. Of course, there are plenty of organic reasons to develop tunnel vision and the differential should be stratified along the duration of symptoms. There seems to be no proper literature on this neuroophthalmological classic, except for the few sentences every textbook spends on psychogenic visual field disturbances. Here is what I came up with after reading case reports:

Functional cerebral

  • Psychogenic
  • Migraine

Vascular (see below for a more extensive discussion)

  • Bilateral PCA stroke – typically post top-of-the-basilar
  • Hemodynamic disturbance in the vertebrobasilar area, when no posterior communicating arteries are present
  • Near death experience in cardiac standstill

Ocular

  • Retinitis pigmentosa
  • Chorioretinitis
  • Glaukoma
  • Pseudotumor cerebri
  • AION

Chiasma lesions (produce incomplete tunnel vision)

  • Pituitary adenomas

 

A few words on macular sparing field defects: the literature is not consistent about the anatomical and physiological basis of this phenomenon. Yet it exists. Several explanations have been put forward.

  1. Artifact: it might be an artifact due to the way field defects are proven – perimetry. But more advanced methods tend to also show macular sparing.
  2. Retinal overlap: both retinal hemifields might give have fibers of the other halves’ macular region – this is very hard to prove.
  3. Bilateral representation: this should be due to an early crossing branch of the optic tract or radiation.
  4. Vascular: myth has it that the occipital pole is supplied by early branches of the PCA or branches of the Sylvian artery (coming from the MCA). While the latter seems to be rare in the only existing studies (see reference below), the former could be more frequent. The visual cortex is supplied by  four main branches of the PCA: the anterior and posterior temporal arteries, the parietooccipital artery and the calcarine artery.

Reference: here is a cool article on the history and theory of macular sparing.