Bainbridge vs Bezold-Jarisch reflex – who wins in neurocardiogenic syncope?

The original tracing of the bainbridge reflex
The original tracing of the bainbridge reflex

About a century ago, Bainbridge described his reflex (if not under that name), namely increase of heart rate provoked by increased venous return. Although it has long been debated how big a role it plays in human vs. canine physiology, it is the physiologic foundation for respiratory arrhythmia, the effect of metronomic breathing on heart rate (as measured during autonomic testing) and many more phenomena.

In neurocardiogenic syncope it might play a role in the final bradycardic phase, but more likely is that it is far overtaken by yet another physiologic (and similarly controversial) reflex named after Bezold and Jarisch.

If all that confuses you, then take a look at this recent anesthesiologic article.

Blood pressure management in ischemic stroke

I have been on conferences and other meetings the last two weeks, which is why I didn’t write anything.

Back on track, we go back to the roots of a proper stroke physician: blood pressure management. We discuss the physiology and pathophysiology of autoregulation and it’s impairment in the penumbra of a stroke (regardless of whether it is small – a lacune – or big – an embolic stroke, there is always an area of tissue at risk around the stroke core). Depending on the time and place you measure it, brain tissue might like more or less of blood (flow or pressure); if it is not enough, ischemia develops, otherwise the breakthrough edema happens (as in RPLS aka PRES). If the local tissue pressure is too high (e.g. through edema), perfusion pressure needs to be higher than in areas where no pressure has developed.

All in all, you never know the distribution of pathophysiological processes and therefore you can never know the best blood pressure for your stroke. Now, if recanalization happens this doesn’t really matter much as the penumbra (hopefully) shrinks to nil, which is why this should be our primary goal. Otherwise or on the way to recanalization we compromise:

  • Don’t change blood pressure – you never know where it should be.
  • In extreme cases (> 220/110 mmHg) you are allowed to lower the blood pressure carefully (slowly) about – say – 20%
  • rtPA/recanalization: if you thrombolyse or try to mechanically recanalize, reduce RR to below 160 (as a goal, which means you arrive at 180 proper) to prepare for the time of recanalization (which you can never pinpoint)
  • After recanalization: breakthrough edema is dangerous, reduce RR to below 140 (as in post-CEA or post-stent)
  • If the acute phase is over (no tissue at risk left): wait for the natural fall of RR (roughly 7-10d)
  • Then (ambulatory care!) aim at < 140/90 mmHg; no particular preference for any substance class
  • For systolic hypertension w/o AI try thiazides.
  • For labile and office hypertension try Ca-antagonists



Fever is an often raised problem in neurocritical care and stroke medicine. Here are some notes from todays lecture.


  • Infectious causes
  • Drugs (PHE, allopurinol, heparin, minocycline, neuroleptics, serotonergic)
  • other central fever forms (in particular in SAH: impending vasospasm), localizing to the hypothalamus, the third ventricle or the pons.

Management. Regardless of your threshold for fever or hyperthermia, you need to work it up systematically.

  • History: course of fever, is it still rising, drugs
  • Examination: is the body trying to heat or cool (is it fever or hyperthermia?)
  • Examination: sources of infection
  • Labs: apart from the obvious, think of troponin and procalcitonin (the latter if sepsis is assumed)

Therapy. There are some contexts in which fever or hyperthermia is not to be tolerated: stroke, MI, non-stable tachyarrhythmia. Remember that in the case of sepsis, it is probably better tolerated.

In the case of stroke, we know the following:

  • temperature is bad (outcome and mortality-wise)
  • it is safe to try to lower temperature (cf. PAIS study)
  • it is hard to lower temperature (the Kallmünzer/Kollmar publications)

It is not really clear

  • whether it really helps to lower temperature
  • what threshold to use
  • what methods are efficient

In our Stroke Unit, we decided to introduce a 3 layer approach:

  • 37,5°C: low-dose paracetamol or metamizol (4 x 500 mg)
  • 38°C: physical cooling and high dose (4 x 1000 of either)
  • 38,5°C: combination therapy and forced physical cooling
  • 39,5°C: desperate measures

Desperate measures, in particular for central dangerous fever (> 40°C)

  • Dantrolen
  • Baclofen
  • Lytic cocktail (block any neurotransmitter that might be involved in fever generation; since we don’t know which might be, block all of them) using anticholinergically acting neuroleptics + antihistamines + antiserotonergics + pethidine


In general, medical students suffer a lot through bad education. Neurology adds to this the very special Neurophobia.

In my quite personal opinion, a lot could be improved if we actually knew what students should do and learn in our hospital. Is it history taking and (neurological) examination? Bedside manners? Basic Neurology? Advanced Neurology? Fascination for the field? The dreadful everyday life of a doctor?

Further confusion comes from the fact that we happily deploy medical students for some tasks (phlebotomy in some hospitals, mini mentals, walking speed measurements, writing discharge letters) that we really don’t like to do ourselves.

The “Junge Neurologen” is an initiative of not so young Neurologists trying to improve education and career options for Neurologists-to-be in Germany. Valuable!

Of course, we cannot simply revolutionize the way our medical education and system works, but there are some messages I’d like to convey:

  • Students are there to learn basic stuff, core skills (history, examination, localization, differential) and bedside manners.
  • They should treat patients (themselves, that is).
  • They should love their time on our ward – what we don’t like, they won’t. What we didn’t like then, won’t be that great today.
  • They should be and feel responsible.
  • They should respect the basic virtues of punctuality, politeness and preparedness – if they don’t, teach them to.
  • You should fetch them from where they are: how far are they? what do they know? what do they want to learn?
  • Don’t show them how bad medicine can be, show them how great it is.
  • Avoid Neurophobia by concentrating on common diseases, on basic skills, normal examination techniques, standard examinations and keep from rare three-eponym-diseases in your differential, weird examination techniques no one can recognize.

References: the only international journal that regularly issues articles on medical education in Neurology is Practical Neurology – here are some pearls:

Wernicke’s take on Wernicke’s encephalopathy

When I read this case report, I had to smile a bit. Not that it is not worth publishing, but you would expect the authors to look up Wernicke’s original description of what we nowadays call his encephalopathy (mind you, he was of sound mind). We use this trigger to read the excerpt of Wernicke’s Neurology textbook as available online here in his Lehrbuch der Gehirnkrankheiten (vol 2/3, p. 232, for those of you who don’t like to read german, try this translation), where he describes in 3 cases of his own and one french case the precise clinical appearance as well as the pathological peculiarities of the disease, of which he could not know the etiology. In his summary he writes

Es handelt sich um eine selbstständige, entzündliche, acute Kernerkrankung im Gebiete der Augenmuskelnerven, die in der Zeit von 10-14 Tagen zum Tode führt. Die Herdsymptome bestehen in associirten Augenmuskellähmungen, die rasch entstehen, fortschreiten und schliesslich zu einer fast totalen Lähmung der Augenmuskulatur führen; doch bleiben selbst dann noch gewisse Muskeln davon ausgenommen, wie der Sphincter iridis oder Levator palpebrarum. Der Gang der Kranken wird taumelnd und zeigt eine Combination von Steifheit mit Ataxie, die am meisten an die Ataxie der Alkoholiker erinnert. Die Allgemeineerscheinungen sind sehr auffallender Natur und bestehen in Störungen des Bewusstseins, und zwar entweder von Anfang an Somnolenz, oder einem Schlussstadium der Somnolenz, das durch ein länger dauerndes der Agitation eingeleitet wird. Ausserdem war allen 3 Fällen eine Theilnahme der Sehnerven und zwar entzündliche Veränderungen der Papillen eingenthümlich. Stets waren schwere Schädlichkeiten dem Ausbruch der Krankheit vorangegangen, das eine Mal eine Schwerfelsäurevergiftung, die mit Stenose des Pylorus geheilt war, in den beiden anderen Fällen ein Alcoholmissbrauch ungewöhnlich starken Grades. Die Frage, ob in diesen letzteren die Erscheingungen des Delirium potatorum als Complication oder als selbstständige, dieser Krankheit zukommende Allgemeinerscheinung aufzufassen sei, kann wohl aufgeworfen, aber nicht entscheiden werden, jedenfalls lag nicht ein gewöhnliches, sondern mindestens ein mit den Symptomen der Poliencephalitis complicirtes Delirium tremens vor. Doch mag darauf hingewiesen werden, dass die characteristische Unorientirtheit auch in dem ersten Falle constatirt wurde, dessen Erscheinungsweise von der des Delirium möglichst weit entfernt war. Nachdem die erste Beobachtung bei Lebzeiten ganz unverstanden geblieben war, gelang es mir bei der zweiten und dritten trotz der Abweichung in den Allgemeinerscheinungen die Diagnose zu stellen. Daraus folgt wohl die Berechtigung diese Fälle als ein besonderes Krankheitsbild hervorzuheben.

This would be translated as

What is present is an independent, inflammatory, acute nuclear disease in the area of the nerves of the eye muscles,
leading to death in a period of 10–14 days. The focal symptoms consist of associated paralyses of the eye muscles, which rapidly arise, progress and finally lead to almost total paralysis of the eye muscles; but even then with the exception of certain muscles, such as the sphincter iridis or levator palpebrarum. The patient begins to stagger when walking and his gait shows a combination of stiffness and ataxia, which is most reminiscent of the ataxia of alcoholics. The general signs are very striking and consist of alterations of consciousness, either somnolence from the outset or a final phase of somnolence preceded by a longer phase of agitation. In addition, in all three cases the visual nerves were affected, with inflammatory lesions of the papillae. In every case the onset of the disease had been preceded by taking harmful substances, in the one case sulphuric acid poisoning, which had healed [leaving?] pyloric stenosis, in the other two cases an uncommonly high level of alcohol abuse. The question of whether in these latter cases the signs of delirium potatorum should be regarded as a complication or as a separate general manifestation pertaining to this disease may be posed but cannot be decided; at any rate what was present was not an instance of common delirium tremens but, at the least, delirium tremens complicated by the symptoms
of poliencephalitis. However, it should be pointed out that the characteristic disorientation was also observed in the first case, the features of which were totally different from those of delirium [tremens]. Whereas the first observation had not been at all understood while the patient was still alive, in the second and third cases I was able to make the diagnosis despite the difference in the general signs. I think that this provides a justification for drawing attention to these cases as [representing] a particular syndrome.

What can be learned from that? See one new disease and be able to recognize it in the next patient in order to diagnose it? Write up detailled descriptions of your patients and their examination? Read old textbooks, because they are written well and very instructive?

I think that all of that is true.

What’s up in CTS?

For hospitalists CTS is a rare diagnosis, but still I retain my fascination for this all but ubiquitous disease. Most of what there is to know can be found in any good textbook on the subject and our new guidelines, so we concentrate on neuroanatomy, surgical techniques and injection technique, using this video on endoscopic surgery and this video on (one approach) to injection and this video for using ultrasound for injection.

Let me mention in passing a few recent papers I stumbled upon that might be of interest: