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Carotid Sinus reflex death - a theory and its history


The number of errors in any piece of writing rises in
proportion to the writer's reliance on secondary sources.
Faber's Law


Whether it is likely or not to die a "sudden cardiac death" from stimulation of the carotid sinus may be more important to breath control practitioners than to anyone else. I did this research because of my growing dissatisfaction with the evidence provided (or, more often than not, not provided) by authors of BDSM safety tips who claim that there is a dire risk of carotid sinus reflex death in breath control play. While some authors at least try to explain the underlying mechanisms, others merely give abridged and sometimes ludicrously wrong descriptions of the "lethal carotid sinus reflex". These misunderstandings have pervaded BDSM literature as well as medical and psychological literature on breath control play to an astounding degree. A closer look at the forensic and medical literature yielded, in short, this:

Now for the details. Caution: The material collected here may seem extremely boring to some readers. You have been warned :-)


Tardieu & Brouardel

Some cases of Tardieu and Brouardel from around 1870 are frequently referred to:

Tardieu told of an old woman who sold snuff to a little urchin. While he was waiting for the snuff the boy attracted by the sight of the old woman's Adam's apple moving up and down in her neck, struck her a blow on the larynx as if he were trying to catch a butterfly. The woman died instantaneously.
(Brouardel, P. (1900): Death and Sudden Death, p. 192, cited (and translated) in Bow62)

A man during conversation gave his wife a shove to the neck to push her back. Immediately, the woman dropped to the floor and was dead "soon afterwards". No evidence that more violence had been used could be found.
(Kaiser claims to cite this case of Brouardel's from Bow62, where it is not mentioned, though.)
(Kai67, translation KP)

Reflex deaths due to "larynx shock" have been described in literature a little more frequently than carotid sinus reflex deaths. There appear to be major objections to this explanation as well (MO82, BP90), but I have not looked into this in detail and do not know whether research on that point is as fishy as on carotid sinus reflex death. The mechanism, however, is not quite the same as in carotid sinus death and the two should not be confused.

Brouardel, who mentions these cases together with some others, relates the story of a priest who was 'obliged to remove his mistress from his vicarage. Everything was made ready for her departure, said the priest, the sorrow had broken my heart, and I said to her:
'We should be happier if we were dead.'
'Yes,' said she, 'if we could die together,'
I then said to her jokingly, for I could find no other way of expressing myself at that moment:
'Could you bear me to cause you much pain?'
'Try,' she replied.
'We were both standing up. I grasped her neck. It was intended as a harmless piece of pretence on my part, and she showed by a smile that she regarded it as such. All at once she made a gesture of pain and shook her hands, but without uttering any cry. I relaxed the pressure, and she fell down. I picked her up, but she was dead.'
(Brouardel, P. (1900): Death and Sudden Death, p. 192, cited (and translated) in Bow62)

A Le Mans shoemaker who had an argument with a young girl gripped her neck with his left hand, as he was working with his right, without exerting undue pressure, and shook her somewhat. She drops to the floor backwards, her body twitches a little, she is dead. He claimed that he had had no intention of killing her. At autopsy a bloody swelling on the back of the head was found, superficial little abrasions at the larynx, 2 on the left side, 6 on the right side. The forensic pathologist at Le Mans argued that the girl had been purposefully strangulated, Brouardel claimed that death was due to "inhibition laryngée" in the way described by the defendant. The pathologist based his view on the presence of foam at the mouth, congestion of lungs and heart, the presence of subpleural emphysema and ekchymoses, the absence of Blutgerinnsel in the heart. Brouardel holds the view that all these signs are neither proof of manual strangulation nor disproof of reflex death.
(Str08, translation KP)

This case would certainly not be regarded as a reflex death today.


Lochte 1930 ("Fall von Dielingen")

Die Dienstmagd H. aus Gr. wurde seit dem 17. XI. 1925 abends vermißt; am folgenden Tage wurde die Leiche im sogenannten Grenzgraben (...) gefunden. Die Leiche lag mit dem Gesichte auf der Sohle des Grabens, die Beine waren an der Oberfläche des Wassers sichtbar. Die H. war im 8. Monate schwanger, als Vater des zu erwartenden Kindes hatte sie wiederholt den v.D. bezeichnet. Einige Tage vor ihrem Tode hatte die H. an v.D. einen Brief geschrieben, in dem sie ihn der Vaterschaft bezichtigte und gegebenenfalls ein gerichtliches Vorgehen in Aussicht stellte, wenn er seinen Verpflichtungen nicht nachkomme.
(...)
Das Geständnis lautete folgendermaßen:
"Die H. versuchte zunächst sich zu wehren, konnte dabei aber nicht viel ausrichten, weil sie die Arme unter dem Tuche verschrenkt hatte. Ich glaube, daß sie noch versucht hat zu schreien. Daran wurde sie aber gehindert, weil ich ihr das Tuch ganz plötzlich fest unter dem Halse zusammen zog. Dann fiel die H. zu Boden. Sie gab weiter kein Lebenszeichen von sich, als daß sie mit den Beinen noch einige Male strampelte. Dann blieb sie ruhig liegen. Als ich nun einsah, was ich angerichtet hatte und daß die H. tot war (ich nahm wenigstens an, daß sie tot war, da sie keine Lebenszeichen mehr von sich gab) nahm ich die Leiche und warf sie ins Wasser, um dadurch den Anschein zu erwecken, daß sich die H. selbst ertränkt hätte."
(...)
Da damals mehrere andere umfangreiche Gutachten gleichzeitig zu erstatten waren und das Gericht wiederholt auf Erledigung gerade dieses Gutachtens drängte, sah ich mich genötigt, von allem wissenschaftlichen Beiwerk abzusehen und mein Urteil dahin abzugeben, daß ein plötzlicher Herztod aus inneren Ursachen, ein Tod durch Kälteshock oder psychischen Shock, Tod im eklamptischen Anfall, oder durch Lungenembolie nicht anzunehmen sei, weil der Obduktionsbefund dafür keinen Anhaltspunkt gebe und das Mädchen bis zum Tode gesund und arbeitsfähig gewesen sei.
Es sei daher die Frage zu erörtern, ob der Tod gegen gewaltsame Erstickung spreche. Die Erfahrung lehre, daß auch bei gewaltsamer Erstickung das Herzblut geronnen gefunden werden könne. Im vorliegenden Falle komme nicht nur der Gesundheitszustand der betreffenden Person, sondern auch der Zeitpunkt der Obduktion in Betracht, insofern bei sofortiger Obduktion flüssiges Blut, später (am 4. Tage) geronnenes Blut gefunden werden könne. Dazu komme, daß, wenn auch in geringer Menge, Wasser in die Lungen und damit in das Herzblut gelangt und als körperfremde (anisotonische) Flüssigkeit zur Gerinnselbildung Anlaß gegeben haben könne. (...)
Im übrigen konnte bei der Bauchlage der Leiche im Wasser die etwas gedunsene Beschaffenheit der Augenlider und der Unterlippe, eine Blutung in der Übergangsfalte der linken Augenbindehaut, eine Verletzung der Unterlippe auf der linken Seite, die zwischen den Zähnen eingeklemmte und vorgelagerte Zunge, etwas streifige Verfärbung an der Vorderseite des Halses, das Fehlen jeglichen inneren Obduktionsbefundes, insbesondere das Fehlen von Blutungen in der Halsmuskulatur, weder für noch gegen einen Erdrosselungs- oder Würgevorgang verwertet werden.
Tod durch Ertrinken war mit Sicherheit auszuschließen, denn es fand sich an der Leiche kein Emphysema aquosum, keine Tigerung des Lungenfelles. Der Magen war frei von Wasser. Es ließ sich also weder Aspiration von Wasser noch Verschlucken von Wasser nachweisen.
Das Mädchen mußte demnach tot oder fast tot in das Wasser hinein gelangt sein. Entscheidend war nach alledem die Frage, ob der negative Obduktionsbefund in Einklang sei mit dem Geständnis des v.D. Diese Frage habe ich auf Grund der mir bekannten Literatur bejaht und mein Gutachten dahin abgegeben, daß der Obduktionsbefund nicht gegen gewaltsame Erstickung spreche und der Leichenbefund im Einklang mit dem Geständnis des v.D. sei.
Von der Verteidigung wurde nunmehr ein Gutachten von Herrn Geh. Rat Strassmann eingeholt.
Strassmann legte in seinem Gutachten eingehend dar, daß Drossel- oder Würgemerkmale am Halse der Leiche der H. weder außen noch innen feststellbar waren, und daß daher ein sicherer Beweis dafür, daß der Tod der H. durch eine Erdrosselung oder eine Erwürgungshandlung erfolgt sei, zweifellos durch das Obduktionsergebnis nicht erbracht sei. Nun hat der Angeklagte hier ein Geständnis abgelegt. Bringt man dieses Geständnis in Beziehung zum Obduktionsbefund, so ergibt sich, daß der Angeklagte die H. nicht stark und nicht lange am Hals gepackt und das Halstuch zugezogen haben kann. Die H. muß vielmehr sehr rasch auf das Zupacken am Halse zusammengebrochen, bewußtlos geworden und gestorben sein. Nur hiermit ist der Obduktionsbefund, die eigenartige Armhaltung der Leiche im Wasser mit noch um die Ellenbogen geschlagenen Tuchzipfeln, das auf ein Fehlen jeder Abwehr hindeutet, sowie das Fehlen von Abwehrverletzungen zu erklären.
Auch die Schilderung der Vorgänge durch v.D. stimmt damit überein, denn die H. ist nach dieser nicht langsam, alle Phasen des klinischen Erstickungsvorganges zeigend, sondern offenbar sehr rasch gestorben. Es müssen daher beim Tode der H. außer dem Zupacken am Halse - ob es nun mit einem Drosseln oder Würgen verbunden war - ist belanglos, außerdem noch andere Momente eine Rolle gespielt haben. Welche Art dieselben waren, läßt sich nur vermuten; vor allem ist hier an eine Shockwirkung zu denken. Die Situation war für die Entstehung starker Aufregungen und Schreckwirkungen zweifellos sehr geeignet. Ob bei einer gründlicheren Obduktion oder durch eine mikroskopische Untersuchung der inneren Organe, sich irgend welche krankhaften Verwendungen hätten finden lassen, muß dahingestellt bleiben.
Der Zustand der weit fortgeschrittenen Schwangerschaft mit ihrer grundlegenden Umstellung der Körperfunktionen, vor allem auch der nervösen, läßt es durchaus möglich erscheinen, daß die H. infolge des Schreckes durch bloßes Zupacken am Halse rasch sterben konnte, wobei an eine Reizung des Nervus laryngeus superior wenigstens auch gedacht werden muß.
(...)
Schließt das Fehlen einer Drosselmarke am Halse aus, daß die Drosselung des Halses der H. in der von D. geschilderten Weise geschehen sein kann.
Diese Frage muß unbedingt verneint werden. Trotz Drosselung können anatomische Merkmale fehlen.
Es braucht in dieser Beziehung nur an den Tod durch Erhängen erinnert zu werden. Bei dieser sehr häufigen Todesart kann an der Leiche die Marke am Halse durchaus fehlen.
Was für den Erhängungstod gilt, muß aber auch für den selteneren Erdrosselungstod zugestanden werden.
(...)
Allgemein bekannt ist nur das eine, daß bei Anwendung eines breiten, weichen Werkzeuges die Strangmarke fehlen kann, also z.B. bei Anwendung eines Schales, eines gepolsterten Lederriemens, einer Serviette, eines Handtuches usw.
Dazu dürfte dann aber weiter kommen, daß auch dann, wenn das weiche breite Werkzeug nur sehr kurze Zeit eingewirkt hat, die Strangmarke fehlen kann. Das ist eigentlich selbstverständlich. Dieser Punkt ist aber von Wichtigkeit, gerade im Hinblick auf das Geständnis des v.D.
Denn es ergibt sich daraus mit absoluter Sicherheit, daß bei dem von v.D. geschilderten Vorgehen die Strangmarke fehlen konnte, ganz besonders wenn man bedenkt, daß die Obduktion erst 4 Tage nach Eintritt des Todes vorgenommen worden ist.
(...)
Es fragt sich nunmehr, ob Erdrosselungsfälle vorkommen, in denen Blutungen im Bereiche des Gesichtes und Halses fehlen.
Die Durchsicht der Literatur läßt unschwer erkennen, daß alle Übergänge in dieser Beziehung vorkommen, daß die Blutungen in jedem Grade und an jeder der bezeichneten Stellen vorkommen oder auch fehlen können und daß gelegentlich auch der ganze Obduktionsbefund negativ oder nahezu negativ sein kann. (Vgl. Haberda, Lehrbuch der gerichtlichen Medizin 1927, S. 698.)
(...)
In der Literatur ist ein Fall von Brouardel bekannt, in dem die Gewalteinwirkung nicht in Würgeversuchen, sondern nur in einem Stoße bestand, den ein Mann im Verlaufe der Unterhaltung gegen den Hals eines Mädchens ausführte, um sie zurückzustoßen. Unmittelbar danach fiel das Mädchen bewußtlos um und war bald darauf tot. Hier waren keine Spuren einer stärkeren Gewalteinwirkung nachzuweisen und Brouardel nahm Kehlkopfshock als Ursache des Todes an. Ziemke sagt hierzu in Schmidtmanns Handbuch der gerichtlichen Medizin (Neunte Auflage 1907, S. 295): Der plötzliche Tod ist in diesem Falle wohl nur als reflektorisch ausgelöste Folge einer stärkeren Laryngeusreizung aufzufassen; einzige Zeilen weiter fährt dieser Autor fort: "Ein reiner Reflextod durch Laryngeusreizung gehört jedenfalls zu den recht seltenen Ereignissen, und wenn nicht andere Umstände dafür sprechen, wird man im allgemeinen derartige Angaben als wenig glaubhafte Ausflüchte abzuweisen haben."
(...)
Durch diese Erwägungen, die ich nicht mit in das Gutachten aufgenommen habe, weil sie nur eine Vorarbeit zum Gutachten darstellten, weil sie in der Literatur ihre Stütze finden und den Gutachtern zugänglich waren; bin ich zu der Überzeugung gekommen, daß die Annahme eines gelegentlich vorkommenden schnellen Todes durch Einwirkung auf den Hals keine Legende ist, sondern wissenschaftlich wohl begründet und durch die praktische Erfahrung (vgl. die Fälle von Brouardel und Strassmann) bestätigt wird.
(...)
Das Urteil erging dahin, daß v.D. wegen Körperverletzung mit Todeserfolg zu 2 Jahren Gefängnis verurteilt wurde.

(Loc30)


Dyrenfurth and Steinbiß 1930 (a comment on the "von Dielingen" case)

Eventually we summarized our expert opinion thus:

  1. In agreement with the pathologists and the authors of the first expert opinion: The autopsy results have failed to clarify the cause of death.
  2. The findings are not inconsistent with the assumption of death by violence, but cannot be used to support it either.
  3. Unfortunately the autopsy report shows certain imperfections that leave a wide scope for criticism regarding a possible death from natural causes.
  4. The assumption of death by cardiac arrest according to Dr. Bonne's theories must be rejected.
  5. At this stage, von Dielingen's confession cannot be made use of for a medical appraisal.

(DS30, translation KP)


Giese 1930

Eine 24jährige Frau war im November am Straßenrand tot aufgefunden worden. Sie war vollständig bekleidet und hatte um den Hals ein lose sitzendes wollenes Halstuch.
Leichenbefund: An der linken Halsseite 3 linsengroße Hautabschürfungen in der Höhe des Kehlkopfes, von denen die mittlere etwas außer der Reihe mehr seitwärts lag, nicht unterblutet. Keine Stauung in der Gesichtshaut, keine Blutungen in den Augenbindehäuten, ebensowenig in der Schleimhaut der Mundhöhle. Keine Blutungen in der schichtweise präparierten Halsmuskulatur, keine Kehlkopfverletzung. Blutfülle der Lungen und Lungenödem. Im Lungenfell des rechten Lungenlappens Ekchymosen, auf dem Lungenfell des linken Unterlappens frische, leicht abstreifbare Faserstoffbeschläge. Flüssiges Blut im rechten Herzen und den großen Venen.
Mäßige Blutfülle des Gehirns. Schwangerschaft von 4 Monaten. Sonst kein krankhafter Befund, der für eine Todesursache in Betracht kam, auch kein Status thymicolymphaticus.
Dieses Ergebnis schien dem bei der Leichenöffnung anwesenden Staatsanwalt zu geringfügig, um an einen gewaltsamen Tod zu glauben, obwohl ich ihn darauf hinwies, daß auch durch einen kurzen Zugriff am Halse, worauf die 3 Hautabschürfungen hinwiesen, ein schneller Tod aus nervös-reflektorischer Ursache möglich sei.
Der zur Anerkennung der Leiche anwesende Ehemann, von dem bekannt geworden war, daß er mit seiner Frau in Unfrieden lebte und sie öfter tätlich mißhandelt hatte, hatte bisher jede Mitwirkung am Tode seiner Frau bestritten.
Nach Schluß der Leichenöffnung tat ihm der Staatsanwalt Vorhalt im Sinne meiner ihm gegenüber erwähnten Möglichkeit eines schnellen Todes durch Zugreifen an den Hals, und nun legte er folgendes Geständnis ab: Er befand sich mit seiner Frau auf der Landstraße auf dem Heimwege. Wie schon oft, sei es zu einem heftigen lauten Streit gekommen, da habe ihn die Wut gepackt und er habe sie am Hals gekriegt. Die rechte Hand sei an der Kehle gewesen, die linke am Genick. Er habe sie ungefähr eine Minute so gehalten (im Stehen) und zu ihr gesagt: "Bist du nun still?" Seine Frau habe gesagt: "Laß mich gehen." Sie habe das kaum herausgebracht, er habe sie auch gleich losgelassen, sie sei dann röchelnd umgefallen. Er habe sie liegen lassen und sei allein nach Hause gegangen.
(...)
Daß ein Druck auf den Sinus caroticus möglich war, erhellt ohne weiteres aus der Lage der 3 Druckmarken. Daß diese nicht stärker ausgebildet waren, erklärt sich durch das Halstuch, das die Frau trug.
Durch den Zugriff mit beiden Händen war weiterhin ein Verschluß der Halsschlagadern und beginnende Erstickung möglich, also die Vorbedingungen, die Koeffizienten Herings für eine Steigerung des Carotisdruckreflexes, der zu Herzkammerflimmern führte, gegeben. Als weiteren Koeffizienten bin ich geneigt, die frische Rippenfellentzündung anzusehen, während ich hinsichtlich der Bewertung der Schwangerschaft Lochte beipflichte.
(Gie30)


Gardner 1942

There is, however, another possible factor not often considered in this country [Britain, K.P.] as contributing to sudden death but more frequently invoked on the other side of the Atlantic. (...) I think that the carotid sinus is worth some consideration as a factor in causing sudden death, because splits are sometimes found in the lining of the carotid artery at its bifurcation, or across the carotid sinus, indicating pressure of the rope, and further it is quite certainly the area that is sought for and compressed in certain knockout holds in jujitsu exercises. I have had long talks with a Japanese instructor of jujitsu well known in London, and he had no doubt about this. He explained that it would be possible to compress the common carotid arteries below their bifurcation, but this would necessitate the use of two hands, whereas the hold on the sinus is made with the fingers or thumb of one hand. He told me he could render anyone unconscious in 3 seconds or kill him in 20 with pressure on the sinus, and he passed a silk belt about 2 inches wide across the back of my neck and brought the ends in front; then holding one he pressed the other against the side of my neck high up under the angle of the jaw, and as far as unconsciousness went he spoke truly, but I think it happened in under the 3 seconds.
(Gar42)

This unconsciousness could, as the other texts will show, only have been due to carotid sinus reflex if Gardner had the - very rare - condition of carotid sinus hypersensitivity or else was suffering from severe arteriosclerosis due to old age at the time of this experiment. Unconsciousness does set in 3-10 seconds (DM88, DiM89, MD90) when the carotid arteries are completely occluded. From Gardner's description of the experiment it is not clear whether his losing consciousness might not rather have been due to this mechanism, which is far more likely (but was not very well known in 1942, as most research on the phenomenon wasn't done until much later)


Simpson 1949

In another case a soldier on leave was dancing with a girl, when he edged her to a corner and, placing his hand across the front of her neck, he "tweaked it playfully" - a mere momentary tightening. She immediately collapsed to the floor, lay still, and did not draw another breath: she was dead.
(Sim49)

This is - as far as my research goes - the first time this "soldier on leave" case is mentioned. (The "other" case Simpson refers to wasn't about carotid sinus reflex death.) I have not yet been able to find out more details about this case, and Simpson does not give any references.


Camps / Hunt 1959

It has been recognized for a considerable time that a nervous stimulus can cause rapid death, and Casper (Casper's Forensic Medicine, 1862) stated that death from suffocation could happen rapidly from 'nervous apoplexy'  in which there was no trace discoverable by the anatomist's knife. This form of reflex, commonly called 'vagal inhibition', which we prefer to call 'reflex cardiac arrest', is probably initiated by alteration in carotid sinus pressure, the vagus nerve trunk in man being comparatively inexcitable to mechanical stimulation. Carotid sinus stimulation in man can produce effects varying from transient cardiac slowing, hypotension and vasodilation, to syncope, cardiac arrest and possibly death. Very marked cardiac slowing can be produced in arteriosclerotic subjects, but unfortunately there are no records available to show whether strangulation in older people with carotid artery atheroma produces more rapid death.
(CH59)


Bowden 1962

On one occasion a young soldier was arrested and charged with the murder of a young woman in the following circumstances.
He said that after a dance to which the young woman accompanied him, he was walking home with her and suggested intercourse, to which she agreed. During the act he placed his hand on her throat with no intention whatever of harming her, and she went limp, suddenly and was dead.
He made a detailed statement to the police, which the defence alleged the police had fabricated. There was one sentence in the statement which strongly suggested that his story was true, and that was the admission that when he placed his hand on the young woman's throat, she just went limp and was dead. That is what, in fact, does happen and it seemed very unlikely that a policeman in fabricating such a story would be likely to include such a happening.
(Bow62)

How likely is it that there are two separate cases with such striking similarities? I'm still trying to find out more about this mysterious story, but I'm quite certain this is the same case Simpson (Sim49) is talking about, the most important difference being that the girl died on the dance floor in Simpson's version and during intercourse in Bowden's. Bowden gives some more details; however, same as Simpson, he doesn't tell us where he got them from.


Olbrycht 1963

S.P. ein 44jähriger, in starker manischer Erregung tobender Mann wurde zeitweilig in einem primitiven, in einer Scheune eingerichteten Dorfarrest unter ständiger Beobachtung untergebracht. Als der Kranke in der Absicht, den Arrest zu verlassen, seinen Kopf in eine zwischen den Balken der Wand befindliche Spalte setzte, glitt er mit seinen Füßen aus und geriet in die abgebildete Stellung. Obgleich seine Bewacher sofort zu ihm liefen, war er schon tot. In diesem Fall sprechen sowohl die Erhängungssituation, aber vor allem die Plötzlichkeit des Todeseintrittes dafür, daß nicht die Drosselung der Halsarterien, sondern ein Reflextod vorlag.
(...)
Aber aus unserem Institut in den Jahren vor dem ersten Weltkrieg erinnere ich mich an Sektionen von zwei Knaben (bedauerlicherweise sind die Protokolle während der Okkupation verlorengegangen). Beim Willkommengruß hob ein Oheim seinen einige Jahre alten Neffen mit beiden Händen an beiden Seiten des Unterkiefers in die Höhe und küßte ihn. Nachdem er das Kind wieder auf den Boden gestellt hatte, bemerkte er zu seinem Erschrecken, daß es tot war. Als der unglückselige Oheim in seiner Verzweiflung der tieftrauernden Familie am Bruder des Verstorbenen demonstrierte, in welcher Weise er das Kind emporgehoben und geküßt hatte, starb auch der andere Knabe. Die makro- und mikroskopischen Untersuchungen ergaben bei beiden Knaben keine Veränderungen. Als Todesursache wurde Schock angenommen. Tatsächlich handelte es sich wohl um einen reinen zum akuten Herzstillstand führenden Reflextod. Heute läßt sich nach Untersuchungen von Hering (Her27), die damals noch nicht bekannt waren, der Tod beider Knaben besser infolge der Carotissinusreflexe, die durch den Zug an den Carotiden bei Emporheben der Knaben ausgelöst wurden, erklären.

(Olb63)


Taylor and Simpson 1965

A soldier playfully "tweaked the neck" of his girl friend with whom he was dancing - in full view of several other people - as they stood facing each other. "She dropped dead". No marks were found, and there were no signs of asphyxiation. A vagal reflex was assumed to have operated.

Taylor and Simpson carefully quote their sources elsewhere in this chapter on asphyxia. They omit all details in this case.

(...)
Reflex vagal inhibition, from pressure on the vagal sheath or carotid bodies has already been described as a cause of sudden collapse - or of collapse and death in strangling. Even stretching of the neck may initiate this reflex, for similar receptor bodies lie over the arch of the aorta. Vagal inhibition is, it seems, more likely to operate when there is sudden pressure or constriction than when the weight of the body is taken up slowly.
An American air lines employee who was known to be most interested in autohypnosis was found dead hanging from a cupboard door in his room at a Kensington hotel. A notebook on autohypnosis by reducing the cerebral blood flow was found nearby. There was no evidence to suggest suicide and a vagal inhibitory collapse was, not unreasonably, assumed to have caused the experiment to end fatally.

But why was it assumed? We learn nothing about any signs of asphyxia or even the autopsy results.

When vagal inhibition plays the deciding role in the causation of death, the features of asphyxiation will not be established, for death will occur too rapidly for suboxia to develop. The amount of pressure may be remarkably little: Burstein and his colleagues have shown (Burstein, C.L., Martin, S.J. and Rovenstone, E.A. (1949). Anesthesiology, 10, 133) that the stimulus required to produce a minimal fall of blood pressure in the abdomen was sufficient to cause immediate cardiac arrest when applied to the neck.
(TS65)

The authors seem to be mistaken - there is an article by Burstein in "Anesthesiology" on page 133, "The utility of intravenous procaine in the anesthetic management of cardiac disturbances", but nothing in the text matches Taylor's and Simpson's summary.


Kaiser 1967

Case 13: A soldier accompanied a girl to a dance. On the way home he suggested intercourse, to which she agreed. During the act he placed his hand on her throat with no intention of harming her. Suddenly she went limp and was dead. The very thorough autopsy did not produce any results.
(Kai67, giving Bow62 as the source. Translation KP.)

Bow62 does not mention any autopsy, let alone a "very thorough" one. Kaiser either made that detail up or he got his sources mixed up again (cf. Brouardel / Tardieu).


Stumpfe 1969

The possibility of death from carotid sinus reflex has been pointed out in forensic literature in connection with death by hanging, manual strangulation and ligature strangulation (DS30, Gie30, Loc30 / Mueller, B.: Gerichtliche Medizin, Springer, Berlin-Göttingen-Heidelberg 1953 / Ponsold, A.: Lehrbuch der gerichtlichen Medizin, 3. Aufl. G. Thieme, Stuttgart 1967 / Pro60). However, none of the described fatalities could be definitely attributed to this reflex.
As the carotid sinus stimulation test is used routinely in neurology and internal medicine (Askey, J.M.: Hemiplegia Following Carotid Sinus Stimulation. Amer. Heart J. 31 (1946), 131 / Silverstein, A., D. Doniger, M.B. Bender: Manual Compression of the Carotid Vessels, Carotid Sinus Hypersensitivity and Carotid Artery Occlusions. Ann. intern. Med. 52 (1960), 172 / Zeman, E.D., S. Siegal: Monoplegia Following Carotid Sinus Pressure in the Aged. Amer. J. med. Sci. 213 (1947), 603) it is important to further investigate these complications.
(...)
Franke (Franke, A.: Über das Karotissinus-Syndrom und den sogenannten hyperaktiven Karotissinus-Reflex. F.-K. Schattauer, Stuttgart 1963) obtained the following results in examining almost 3900 persons:

  1. More than 70% of the examined persons and almost all adolescents under the age of 20 showed insignificant bradycardia.
  2. In 10% the heart rate slowed by 20 beats, blood pressure fell by 10 to 20 mm Hg, heart standstill did not exceed two seconds.
  3. In 10% the heart rate slowed by 30 to 50%, asystole lasted more than two seconds, blood pressure fell by 30 mm Hg.
  4. In the rest heart standstills from three to five seconds and longer occurred, as well as a drop in blood pressure to 50 mm Hg and lower.

(...) Koch (Koch, E.: Die reflektorische Selbststeuerung des Kreislaufes. Steinkopf, Dresden-Leipzig 1931) pointed out that in healthy persons the results are usually very slight or nonexistent.
From the results of different authors' studies (table omitted, KP) we find that up to an age of 40 no significant heart inhibition occurred, whereas with increasing age heart standstills of several seconds resulted. (...) None of the authors reported any fatalities. However, a general application in elderly people is discouraged. In experiments heart standstills of several seconds have been observed.
(...)
These few severe complications following manipulations of the carotid sinus region cannot be attributed to the reflex mechanism, as some time had passed until these events set in. This means that no reflex action had taken place here.
Furthermore, fatalities have been described that have been put down to carotid sinus reflex.
(...)
Discussion of these incidents shows that fatal complications always occured in connection with other severe diseases. The contribution of the disease cannot be isolated from the potential consequences of a carotid sinus stimulation test. The examiner's finger pressure in these cases merely triggers the evolving event that ultimately runs its course independently. These fatalities cannot be blamed on the reflex mechanism.
Finally the the ratio of complications and performed tests has to be mentioned. Franke (Franke, A: Über das Karotissinus-Syndrom und den sogenannten hyperaktiven Karotissinus-Reflex. F.-K. Schattauer, Stuttgart 1963) did not observe any complications in 4500 carotid sinus stimulation tests and neither did Sigler (Sigler, L.H.: Subjektive Manifestation of the hyperactive Carotid Sinus Reflex. Ann. intern. Med. 29 (1948), 687) in 1193. Webster u. Gurdijan (Webster, J.E., E.S. Gurdijan: Observations upon responses to digital carotid artery compression. Neurology 7 (1957), 757) observed only two complications in several hundred experiments. Bender (Silverstein, A., D. Doniger, M.B. Bender: Manual Compression of the Carotid Vessels, Carotid Sinus Hypersensitivity and Carotid Artery Occlusions. Ann. intern. Med. 52 (1960), 172) reported that in several thousand carotid compressions only two unexpected reactions occurred. The authors point out that complications are possible, but very rare.
(...)
A reflex causing cardiac arrest would be unphysiological, as that would mean the death of the organism. The organism at any rate strives to maintain minimal circulation. Considering these physiological facts it should be apparent that an irritation cannot lead to terminal cardiac arrest.
Experiments on whether it is possible to cause death by stimulating the carotid sinus in humans cannot be carried out. Neither, however, are they necessary, as countless experiments on carotid stimulation have been performed and still are being performed. No fatalities have been observed that can be interpreted as consequences of this reflex. These results support our belief that there is no terminal reflex cardiac arrest due to stimulation of the carotid sinus, and that it is not possible to induce reflex death via this mechanism.
(Stu69, translation KP)


Resnik 1972

There is another and more immediate consequence of neck constriction. Bilateral pressure upon the carotid sinus will reflexly result in immediate unconsciousness. Thus, pressure applied slowly to the neck may result in enhanced sensations. When, by inexperience, excitement, or accident, the pressure is sudden or exxagerated, so, too, may be the result - carotid sinus reflex, unconsciousness, asphyxia, and death.
(...)
The real danger appears to be unconsciousness following carotid sinus reflex.
(Res72)


Adelson 1974

Pressure (and other types of stimuli) applied to the neck overlying the carotid sinuses can, in the predisposed victim, initiate catastrophic inhibitory vagal nervous impulses which cause practically instantaneous stoppage of cardiac activity and death, a phenomenon variously termed death from inhibition, nervous apoplexy, reflex cardiac death and instantaneous physiologic death.
Although the stimulus which initiates the fatal vagal reflex can be so atraumatic that it leaves no anatomic changes demonstrable at autopsy, the cardiovascular apparatus of the victim vulnerable to this ordinarily innocuous incident undergoes a hyperacute functional response, characterized by a fulminating sequence of cardiac slowing, hypotension, diffuse peripheral vasodilatation, syncope, asystole and death. Emotional tension is said to "facilitate" the reflex or to heighten the response, a state of affairs certain to be present in a conscious person being assaulted. Such a reflex may be the explanation for an unexpected fatality where the suspect says truthfully, "I just pinched her neck (or squeezed it gently) and she fainted, and I couldn't wake her up."
(Ade74)

Note the passage lifted verbatim from CH59 (or maybe both copied from a third source, I'm still researching). The "unexpected neck-pinching fatality" is probably our "soldier on leave" again.


Knight 1976

However, it must be said immediately that external pressure on the neck by no means causes death solely through an asphyxial process. In fact, probably half such cases* have no asphyxial element, a fact that is not always appreciated. Considerable, sustained pressure is necessary to close the airway by the application of external force. This is not the mechanism that kills many people who have their necks pressed.** In these cases, death may be rapid, sometimes almost instantaneous and is due to reflex cardiac arrest following impact or pressure upon the carotid system of receptors. Either the carotid sinus, carotid body or carotid vessels themselves may trigger autonomic responses sufficient to cause cardiac arrest when the neck is suddenly stimulated, on one or both sides. This is the principle of the 'commando punch' and the various dangerous procedures such as the 'karate chop'. In these instances, there may be no asphyxial element. In other cases, if the initial pressure on the neck has not been primarily over the carotids, there may be the onset of asphyxia, which is then abruptly terminated by a shift of grip so that the carotids are stimulated. Thus a mixed causation of death can sometimes occur, which can be difficult to interpret at necropsy. When a person is found dead with bruises on the neck or when circumstances indicate that he has received some trauma in that region, if the face is pale, there are no congestive signs, no skin or conjunctival haemorrhages, it may well be that death has occurred from this rapid reflex cardiac arrest.
(Kni76)

* Where do the data for the "probably half" such cases come from? No sources are given.
** Indeed it is not. The mechanism that kills most people who have their necks pressed is occlusion of the neck arteries, which is not mentioned here.


Rosenblum and Faber 1979

Unfortunately, while a gradual application of pressure to the neck may result in enhanced sexual sensation, bilateral pressure upon the carotid sinuses will result in immediate unconsciousness due to a reflex drop in blood pressure mediated by the carotid baroreceptors.
(RF79)


Simpson 1979

Many happenings like strangling, or immersion in water, which might precipitate such a course of events, terminate suddenly, often within a few seconds of their commencement, in quite unexpected death before the classical changes of asphyxia can become established. The reason for this is that a vagal inhibitory mechanism supervenes and its effects precede those of asphyxia. Vomit inhalation may also shorten the period of survival.

A woman of 63 died suddenly 'the moment her husband put his hands on her neck - perhaps to threaten to strangle her'. He had cared for her for years, tending her in bed and doing both housework and shopping, receiving little but nagging for his attentions, and his patience broke when, treading on her corn getting her out of bed one day, he was called a 'clumsy blundering fool'. Autopsy showed no evidence of asphyxia and the medical evidence for the prosecution went far to support the defence that death was sudden, unexpected and quite unintended.

Prostitutes and others, raped, or gripped by the neck in a struggle to effect a pinning hold, often die unexpectedly in the passion of the moment, and autopsy may give good reason to believe that death ensued suddenly. Phrases like 'I gripped her by the throat and she suddenly went limp' ... 'I tried to bring her round, but she was dead' afford good evidence of the rapidity with which death may occur. Asphyxial changes in such cases are of a trivial character, or absent altogether.
Many masochistic experiments in binding and hanging in erotic youths end tragically in sudden death as a cord slips and tightens on the neck. A vagal reflex may also cause sudden loss of consciousness so that death follows from asphyxia.

No source for the old woman's case is given in this text, but in TS65 we find that it must have been R. v. Rourke (C.C.C., 1934)


Reay and Eisele 1982

A second factor working to produce cerebral ischemia in the carotid sleeper is carotid sinus stimulation which can produce bradycardia and sometimes cardiac arrest. (...) Massage of one or both of the carotid sinuses (particularly in the elderly) can cause bradycardia and/or a fall in arterial pressure with consequent decrease of blood flow to the brain. Carotid sinus hypersensitivity has been described where syncope has been produced by turning of the head, wearing a tight shirt collar, or by shaving over the sinus region of the neck (Walter, P.E., Crawley, S.I. and Dorney, E.R.: Carotid sinus hypersensitivity and syncope. Am J Cardiol 42: 396-403, 1978) (...) Underlying disease such as coronary artery disease and cardiac rhythm disorders are particularly vulnerable to reflex carotid sinus stimulation and hypoxia (Tho69) (...) Without being all-inclusive and citing rare medical conditions, there are general medical considerations which may be of some use in identifying individuals who are at greater risk of death from a neck hold. These include: 1) Men over the age of 40: The incidence of coronary artery disease increases sharply after the age of 40 and there are asymptomatic men with significant coronary artery disease (Krueger, B.R., and Okazaki, H.: Vertebral-basilar distribution infarction following chiropractic cervical manipulation. Mayo Clin Proc 55: 322-332, 1980). This group would be particularly vulnerable to carotid sinus stimulation and/or hypoxia which could trigger a fatal heart dysrhythmia.
(RE82)


Creighton 1983

Finally, in persons older than 19, there is a third and even more pernicious effect. By that age, arteriosclerotic changes may have begun to develop in the "carotid bodies," located below the angle of each jaw and within the carotid arteries where each divides into two branches. (...) Thus, external pressure from the application of a chokehold will influence the carotid bodies, which in turn will depress cardiac output and may even in extreme cases cause the heart to stop beating. This effect is particularly prevalent in persons more than 19 years old, because by that age the carotid arteries have usually suffered some arteriosclerotic ("hardening") changes, which may result in the carotid bodies overreacting to pressure by sending a much stronger and longer message to the heart, possibly causing cardiac arrest. The condition is further exacerbated in persons with high blood pressure or of advanced years.
Although unilateral carotid body massage, which involves applying pressure to one side of the neck only, is a therapeutic technique used in medicine to slow a fast heart rate, bilateral massage is never applied unless resuscitative equipment is available in case of cardiac arrest. Thus, a bilateral Hadaka Jime chokehold mimics a medical technique considered highly dangerous even when it is administered under the supervision of a licensed physician.
(Cre83)


Hazelwood, Dietz and Burgess 1983

Some unknown proportion of deaths from neck compression occur not as a result of obstruction of blood flow in the blood vessels of the neck but rather from the effects of the neck compression on a pressure-sensitive organ in the neck known as the carotid baroreceptor. (...)
According to Adelson (Ade74), pressure to the neck overlying the carotid sinuses can cause practically instantaneous death "in the predisposed victim" (p. 526). Although we are unaware of solid evidence that individuals differ in their pressure sensitivity, there is evidence suggesting that normal individuals differ in chemical sensitivity and that biological responses to hypoxia may be controlled genetically (...)
Sudden death resulting from pressure on the carotid sinuses occurs through changes in nerve impulses conveyed by the vagus nerve, one of the major actions of which is to slow the heart. Sudden death conveyed through these vagal impulses is variously known as "death from inhibition", "reflex cardiac death", "instantaneous physiological death" (Ade74, pp. 526-527), and death from vagal inhibition.
Death from vagal inhibition has been proposed as a mechanism of sudden death in autoerotic asphyxias for at least thirty years (Gar42). Gardner suggested that the contributory role of carotid-sinus pressure in sudden death was better recognized in North America than England, though writings of the time do not seem to support that greener-grass view. In any case, Gardner had noticed occasional tears across the carotid sinus in cases of hanging. This observation led him to consult a Japanese instructor of jujitsu in London about the "knockout holds" in jujitsu exercises.

... He told me he could render anyone unconscious in 3 seconds or kill him in 20 with pressure on the sinus, and he passed a silk belt about 2 inches wide across the back of my neck and brought the ends in front; then holding one he pressed the other against the side of my neck high up under the angle of the jaw, and as far as unconsciousness went he spoke truly, but I think it happened in under the 3 seconds.(Gar42)

(HDB83)


Emson 1983

Hypoxia is commonly induced by partial neck compression; this may act via carotid insufficiency, carotid sinus reflex, or airway obstruction. Loss of consciousness leading to sustained hypoxia and accidental death appears to occur without sufficient warning for the victim to free himself, from cerebral hypoxia, vagal inhibition, or carotid sinus reflex.
(...)
Autopsy showed the ligature mark. There was no other significant finding in the skin, deeper tissues of the neck, larynx, or associated structures, and no evidence of trauma. The only other positive findings at autopsy were slight pulmonary edema (lung weights 470 and 500 g), a small crop of petechiae on the epicardium (...) Postmortem toxicology yielded a blood alcohol level of 130 mg / 100 ml; no other drugs were detected on drug screen.
(...)
Full circumstantial investigation yielded no other significant findings, and the death appeared to be established as accidental from vagal inhibition and anoxia during masturbation under restraint in this most unusual location.
(...)
Death occurring suddenly, and with minimal or no physical findings, has been reported following various manipulations of the neck, usually when the victim is in a state of fear or excitement. Such mechanisms are obviously most difficult to demonstrate and prove, and the underlying cause is probably carotid sinus reflex and vagal inhibition.
(Ems83)


Minyard 1985

This was also a topic discussed by Prof. Leopold Breitenecker, late professor of legal medicine of the University of Vienna, Austra, in his lectures. Pressure on the neck during intercourse was practiced and occasionally resulted in deaths of one of the partners due to the effect on the carotid sinus.
(Min85)

I haven't yet been able to find any written material of Prof. Breitenecker's on this topic. As the few documented cases of death during breath control play with a partner haven't been put down to the "effect on the carotid sinus", it isn't very likely that his cases were any different - if there are any cases and the material is not merely anecdotal again.


Polson, Gee and Knight 1985

In a considerable proportion of deaths from mechanical asphyxia in the Cardiff area, the immediate cause of death was sudden cardiac arrest. Knight found that slightly more than 50 per cent of cases of constriction of the neck (manual and ligature strangulation, choking and hanging) showed no congestive, cyanotic nor haemorrhagic stigmata. These deaths were thus ascribed to rapid death from cardiac arrest. Karate blows to the neck, mugging and some cases of drowning also may cause sudden death from acute cardiac arrest.
An accurate history of the circumstances of death is important. Sudden collapse and loss of consciousness is an outstanding feature but cessation of breathing, or pulse and the heart beat may nut occur until 15-30 seconds have elapsed. There may be ventricular fibrillation, e.g. when electrocuted. If defibrillation is prompt it is possible to restore the patient. Slowing of the heart beat may occur within 90 seconds and this may continue for even a few minutes, with a few bouts of tachycardia before death. (...)
An important feature which supports the diagnosis of acute cardiac arrest, especially in death by drowning, manual or ligature strangulation and karate blows is evidence of surprise, or emotion or apprehension or fright. Alcoholic intoxication is another factor.
A thorough examination of the body is directed especially to signs of injury and its degree of severity. If signs of injury be absent or slight this supports the diagnosis of acute cardiac arrest and a submission that the death was the result of an accident. Normally grave injury favours the allegation of criminal intent. But Knight has examined a number of fractured hyoid bones and horns of the thyroid cartilage, accompanied by haemorrhage, laryngeal mucosal bleeding and skin bruising with no congestive/petechial signs, and yet the history was consistent with rapid death. There is a time interval of from 15-30 seconds available for trauma before there are signs of asphyxia.
(...)
In the event of death from vagal inhibition, unusual in strangulation by a ligature, the signs of interference may be negligible both internally and externally.
It is generally accepted that gross changes, e.g. an obvious mark on the neck, bruising of neck muscles, fracture of the neck structures and obvious signs of asphyxia, are inconsistent with death by inhibition.
(...)
A sudden application of one or both hands to another person's throat is capable of causing sudden death from vagal inhibition, in circumstances which are essentially innocent. The act may be done in jest, or during intercourse, demonstration of affection or it may be part of a physiological experiment. Its dire results are abrupt and injury to the parts is negligible; it is other than accident when death is by asphyxia and there are obvious signs of injury.
This mode of death received attention especially by French medical jurists, notably Tardieu (Tardieu, A (1879) La Pendaison, la Strangulation et la Suffocation, 2nd ed., p. 206, Paris: Baillière) and Brouardel (Brouardel, P. (1897) La Pendaison, la Strangulation etc., p. 228. Paris: Baillière), who described several examples. The cause of death from inhibition in these circumstances was first recognised by Brown-Séquard.

An early, excellent example is that related by Tardieu (1879). A young boy was sent by his father to a neighbouring shop to buy some tobacco. The shopkeeper was an elderly, thin woman whose neck was wasted. The boy, amused at the sight of her larynx ascending and descending with each movement of swallowing, wished to take hold of it "comme il attraperait un papillon qui vole". He sprang forward and struck the woman's larynx and she fell dead.

Another variation of this mode of death was the subject of a murder charge in the United States. A couple were dancing and the man, either playfully or erotically, squeezed the neck of his partner. She went limp in his arms and is alleged to have died instantly. The accused was acquitted of her murder.
(PGK85)

Problems with this text:


Kornblum 1986

This 24-year-old male was sentenced to County jail for drunk driving. Six days later the subject complained of upset stomach, headache and generally not feeling well. He was taken to County hospital for medical evaluation, examined and sent back to jail.
It was suggested at this time that the subject be seen by a psychiatrist. The following morning he was noted to be perspiring and trembling; his eyes were watery; and he was repeating incoherent words. He was observed to be tense and fearful, and had a dazed look in his eyes. He began screaming and kicking; and when the guards attempted to restrain him, a struggle ensued.
Numerous deputies were required to subdue the prisoner. During the course of the struggle, the subject sustained blows to his abdomen, back and neck.
A choke hold was applied by one of the guards. It is uncertain whether a carotid or bar arm type was employed.
During the course of the struggle, the suspect suddenly became limp and stopped breathing.
At autopsy no injuries were found in the neck. No wounds were found of the skin, subcutaneous tissue, muscle, larynx, blood vessels or spine. No petechial hemorrhages were seen, and no signs of asphyxia were noted.
Several small superficial abrasions located on the upper lip, chin, left eye, right wrist and right leg were seen. No other injuries or abnormalities were found.
Toxicological studies were not performed.
The cause of death was certified as sudden death following restraining procedure due to psychiatric disorder, type unspecified. The mode of death was certified as homicide following an inquest.
The death in this case appears to be due to the carotid sinus reflex, complicated by alcohol withdrawal syndrome. There is no evidence for an asphyxial death in this instance.
(Kor86a)


Eriksson, Gezelius and Bring 1987

Hypoxia is most commonly induced by neck compression (by means of carotid insufficiency, carotid sinus reflex, or airway obstruction) (Ems83, HBG81)

Quoted verbatim from Ems83.


Simonsen 1988

Congestion to the face is due to a stronger compression on the neck with the result of blockage of the arteries. A few of those pale faces may be caused by vaso-vagal cardiac shock.
(Sim88)

This is a much more cautious statement than those of Knight's who claims that all of those pale faces are caused by vaso-vagal cardiac shock.


DiMaio and DiMaio 1989

Occasionally, it is claimed that a death ascribed to manual strangulation is unintentional and due to a vasovagal reaction brought on by touching, grasping, or striking the neck. This is theoretically possible, but highly improbable and suspect. The mechanism of death in this case would be an arrhythmia produced by stimulation of the carotid sinuses. The carotid sinus is a focal area of enlargement of the common carotid artery at the point it bifurcates into the external and internal carotid arteries. Compression or stimulation of the carotid sinuses causes an increase in blood pressure in these sinuses with resultant slowing of the heart rate (bradycardia), dilatation of blood vessels (vasodilation), and a fall in blood pressure. Pressure on the common carotid artery below the sinuses reduces the blood pressure within the sinus by reducing the amount of blood flowing into it. This mimics hypotension or decreased blood supply from hemorrhage or shock causing the heart to beat faster (tachycardia), the blood vessels to constrict (vasoconstriction), and a rise in blood pressure. This explains the fact that while in most cases of manual strangulation there is bradycardia, vasodilation, and fall in blood pressure, in some cases, if the hands are lower down on the neck, one may instead have tachycardia, vasoconstriction, and a rise in blood pressure. If minimal pressure on the neck did cause an arrhythmia and death, there would, of course, be no petechiae in the sclerae and conjunctivae.
In normal individuals, pressure on the carotid sinus causes minimal effects with a decrease in heart rate of less than six beats per minute and only a slight reduction in blood pressure (less than 10 mm Hg). Some individuals, however, show extreme hypersensitivity to stimulation of the carotid sinuses. In hypersensitive individuals, there is slowing of the heart and cardiac arrhythmias ranging from ventricular arrhythmias to cardiac stand-still and hypotension. There are cases reported in which turning of the neck in varying positions or a high or tight collar has produced dizziness and fainting. Some articles refer to cases of stimulation of the carotid sinus that have allegedly produced bradycardia, progressing to cardiac arrest and death. Review of the original case reports almost invariably indicates these individuals to be suffering from some severe disease that in itself is capable of causing sudden death.
(...)
Compression of the neck by a carotid sleeper hold may also cause stimulation of the carotid sinus with bradycardia. Application of the hold to an individual who is agitated and struggling may increase the struggling, with increased release of catecholamines. The catecholamines working with the carotid sinus stimulation may produce a cardiac arrest. In addition, if the individual has intrinsic heart disease, he may be even more sensitive to bradycardia and the arrhythmogenic activity of the catecholamines.
(DiM89)


Sigrist, Meier and Zollinger 1989

Der gerichtsmedizinisch tätige Morphologe ist hin und wieder mit Fällen konfrontiert, bei denen der Tod anscheinend rasch nach einem gewaltsamen Geschehen eingetreten ist, die Autopsie jedoch weder schwere Verletzungen noch Krankheiten lebenswichtiger Organe erbringt, wohl aber Befunde, die kennzeichnend für ein rasches Versagen der Kreislauftätigkeit sind. Wenn ich solchen Fällen gleichzeitig reflektogene Zonen verletzt wurden, erhebt sich die Frage nach einem traumatisch ausgelösten Reflextod. Wir haben derartige Fälle beobachtet und möchten darüber berichten.
Im zugänglichen Schrifttum finden sich insgesamt wenige einschlägige Mitteilungen. Erste Berichte stammen von Parry (1799, zit. nach Lewis, T.: Vasovagal syncope and the carotid sinus mechanism. Brit. med. J. i, 873-876 (1932)), Waller (zit. n. Lewis, a.a.O.) und Landois (zit. n. Lewis, a.a.O.). Sie hatten festgestellt, daß der mechanische Einfluß auf die seitlichen Halspartien einen Kreislaufkollaps nach sich zieht; der pathophysiologische Mechanismus war jedoch nicht klar. 1866 vertrat Czermak (Czermak, J.: Über mechanische Vagus-Reizung beim Menschen. Zit. n. Franke, H.: Über das Karotissinus-Syndrom und den sogenannten hyperreaktiven Karotissinus-Reflex. Schattauer, Stuttgart (1963)) die Meinung, daß die mechanische Reizung des N. vagus im Halsbereich für die kardiodepressorische Wirkung verantwortlich sei. Später korrigierte Hering (Hering, H.E.: Die Sinusreflexe vom Sinus caroticus werden durch einen Nerven (Sinusnerv) vermittelt, der ein Ast des Nervus glossopharyngeus ist. Münch. med. Wschr. 71, 1265-1266 (1924)) diese Ansicht; er schloß aus tierexperimentellen Untersuchungen, daß die mechanische Reizung des Sinus caroticus ausschlaggebend ist. In der Folgezeit erschienen etliche Berichte über Todesfälle nach mechanischer Einwirkung gegen den Karotissinus (z.B. Str08, DS30, Loc30, Gie30, Ess33, Simpson (Quelle fehlt, vermutlich Sim49), Olb63; reichhaltige Zusammenstellung publizierter Kasuistik bei Kai67).
(...)
Die Möglichkeit, durch mechanische Reizung des Sinus caroticus reflektorisch eine Bradykardie mit Kreislaufkollaps auszulösen, ist heute unbestritten. Zahlreiche Beobachtungen am Menschen unter experimentellen Bedingungen oder in Zusammenhang mit dem klinisch-therapeutischen Druckversuch z.B. zur raschen Blutdrucksenkung oder zur Coupierung einer paroxysmalen Tachykardie zeigen dies (Franke, H.: Über das Karotissinus-Syndrom und den sogenannten hyperreaktiven Karotissinus-Reflex. Schattauer, Stuttgart (1963) / Nager, F.: Die kardioinhibitorischen Carotissinusdruck-Effekte im Ekg bei Herz- und Kreislaufgesunden. Helv. Med. Acta 28: 42-62 (1961) / Sigler, L.H.: The cardioinhibitory carotid sinus reflex, its importance as a vagocardiosensitivity test. Am. J. Cardiol. 12, 175-183 (1973) / Sunder-Plassmann, P.: Untersuchungen über den Bulbus carotidis bei Mensch und Tier im Hinblick auf die "Sinusreflexe" nach H.E. Hering; ein Vergleich mit anderen Gefäßstrecken; die Histopathologie des Bulbus carotidis; das Glomus caroticum. Z. Anat. 93, 567-622 (1930) / Waller (zit. n. Lewis, T.: Vasovagal syncope and the carotid sinus mechanism. Brit. med. J. i, 873-876 (1932)). Entsprechende EKG-Veränderungen treten schon innert Sekunden nach Reizbeginn auf (Nager, F.: Die kardioinhibitorischen Carotissinusdruck-Effekte im Ekg bei Herz- und Kreislaufgesunden. Helv. Med. Acta 28: 42-62 (1961) . Gleiche Erkenntnisse liegen aus Experimenten am Tier vor (Hering, H.E.: Die Sinusreflexe vom Sinus caroticus werden durch einen Nerven (Sinusnerv) vermittelt, der ein Ast des Nervus glossopharyngeus ist. Münch. med. Wschr. 71, 1265-1266 (1924)).
Geteilt sind die Ansichten über die Frage, ob die reflektorisch ausgelöste Herz-Kreislauf-Depression auch tödlich wirken können. Stumpfe (Stu69) bezweifelt, daß der menschliche Organismus über Mechanismen verfügen soll, mit denen er sich selbst zu Grunde richten könne. Sigler (Sigler, L.H.: The cardioinhibitory carotid sinus reflex, its importance as a vagocardiosensitivity test. Am. J. Cardiol. 12, 175-183 (1973) dagegen meint, daß ein Reflextod möglich sei, allerdings unter der Voraussetzung einer vorbestehenden Herzschädigung.
Demgegenüber stehen die eigenen Beobachtungen. In sechs der sieben Fälle erbrachte die Autopsie keine relevanten pathologischen Veränderungen am Herzen. Dennoch war aufgrund der Gesamtsituation und der Obduktionsbefunde konkret von einem traumatisch-reflektorisch ausgelösten Herzstillstand auszugehen. Vorbestehende Herzerkrankungen scheinen folglich für den tödlichen Ausgang nicht ausschlaggebend zu sein.
Die stattgefundene Traumatisierung der Halsregion war in allen Fällen schon makroskopisch zu verifizieren. (...) In jedem Fall war zumindest eine der Karotisarterien im empfindlichen Abschnitt mechanisch getroffen und dabei lädiert worden.
Die Dauer der Traumatisierung war meist sehr kurz gewesen, was sich aus den Umständen, den Obduktionsbefunden sowie der Tatrekonstruktion ergab. (...) Offensichtlich ist eine persistierende mechanische Reizung einer reflektogenen Zone nicht nötig. Es kann auch ein kurzer Krafteinfluß an entscheidender Stelle ausreichen, um ein tödliches Reflexgeschehen auszulösen.
Die Latenz zwischen Trauma und Todeseintritt war bei den eigenen Fällen - soweit beobachtet - durchwegs sehr kurz. Dies steht in Übereinstimmung mit den im Schrifttum mitgeteilten einschlägigen Einzelkasuistiken (z.B. DS30, Ess33, Gie30, Kai67). Die rasche Abfolge von Gewalteinfluß und anschließendem Kreislaufkollaps ist offenbar ein maßgebliches Kriterium für die Annahme eines reflektorischen Todesgeschehen. Tritt der Tod erheblich verzögert ein, so wird man die Version eines traumatischen Karotissinus-Reflextodes ausschließen dürfen.
Zur kurzen Latenz passen weitere morphologische Befunde, namentlich fehlende oder nur spärliche Zeichen vitaler Reaktion wie etwa Blutungen, Embolien und Aspirationen. (...)
Der Befund einer schwach positiven pulmonalen Fettembolie schließt die Möglichkeit eines traumatischen Reflextodes nicht generell aus, weil vermutlich das Herz nicht schlagartig stillsteht, sondern während einer gewissen wenn auch nur kurzen Zeit noch schwach tätig sein kann. Ist indessen die Lungenfettembolie mittelgradig bis schwer ausgeprägt, so ist von der Diagnose "Reflextod" abzusehen.
Gleiches gilt vermutlich auch für Aspirationen, die aber in unseren Fällen nicht vorkamen. Leichte Aspirationsbefunde stehen nicht im Widerspruch zu einem tödlichen Reflexgeschehen, stark ausgeprägte indessen schon.
(...)
Für den morphologischen Nachweis eines Karotissinus-Reflextodes ist die Untersuchung der Halsorgane, insbesondere der reflektogenen Karotisregionen, durch schichtweise Präparation in sog. künstlicher Blutleere grundlegend; darauf wurde wiederholt hingewiesen (CH59 / MD86 / Merkel, H., Walcher, K.: Gerichtsärztliche Diagnostik und Technik. Hirzel, Leipzig, S. 10 (1936) / Mueller, B.: Gerichtliche Medizin. Kapitel. Tod und Gesundheitsschädigung durch von außen kommende Einwirkungen. Springer, Berlin-Heidelberg-New York, 2. Aufl. (1975)).
(...)
Die Diagnose "Karotissinus-Reflextod" ist grundsätzlich erst nach Ausschluß anderer Todesursachen zu stellen. In Frage kommen natürliche und nicht natürliche (gewaltsame) Ursachen. Herzkrankheiten, speziell Rhythmusstörungen bei koronarsklerotischer Myokardischämie stehen im Vordergrund.
(...)
Nach Darlegung von Natur und Ursache des tödlichen Karotis-sinus-Reflexgeschehens sowie dessen Abgrenzung gegenüber anderen Todesursachen erhebt sich nun noch die Frage nach der Pathogenese.
If the external pressure applied to the neck and the carotid-sinus is no more than negligible, cardiac activity will as rule slow down throughout the duration of the pressure applied. Afterwards the regulatory system recovers its original levels and cardiac activity re-adjusts itself. (Hering, H.E.: Die Sinusreflexe vom Sinus caroticus werden durch einen Nerven (Sinusnerv) vermittelt, der ein Ast des Nervus glossopharyngeus ist. Münch. med. Wschr. 71, 1265-1266 (1924) / Kirchheim, H.: Kreislaufregulation. In: Busse, R. (Hrsg.): Kreislaufphysiologie. Thieme, Stuttgart-New York, S. 167ff. (1982) / Koller, E.A.: Vaso-vagale Komponenten der Lungenreflexe. Bulletin des Schweiz. Bundesamtes für Gesundheitswesen, Beilage "Tuberkulose und Lungenkrankheiten". 1, 1-7 (1983)) By contrast, injuries to the carotid artery wall, as well as intra-mural bleeding, constitute a lasting stimulation of the nerve receptors which persists throughout and beyond the actual moment of traumatisation even though external mechanical pressure and its immediate effects may have ceased. The post-traumatic and persistent stimulation of the pressure receptors therefore appears to be crucial to the perpetuation of the reflexive action and prevents thereby the spontaneous recovery from the reflexively triggered bradycardia (asystole) or periphal vasodilation with circulatory failure, making death the immediate consequence.
(...)
Für die Auslösung des Reflexgeschehens ist nicht nur die Traumatisierung als solche ausschlaggebend, sondern auch die Reflexbereitschaft. Beim sogenannten hypersensiblen Karotissinus-Reflex löst eine verhältnismäßig geringe Traumatisierung bereits das reflektorische Geschehen aus. Dies kommt vorwiegend bei Personen in höherem Alter, mit einer Hypertonie oder mit einem Diabetes mellitus vor, wobei arteriosklerotische Veränderungen entscheidend sind (Franke, H.: Über das Karotissinus-Syndrom und den sogenannten hyperreaktiven Karotissinus-Reflex. Schattauer, Stuttgart (1963) / weitere Quelle fehlt). Eine erhebliche Sklerose der A. carotis war beim eigenen Fallkollektiv vereinzelt nachweisbar (...) In diesen Fällen muß somit die Begünstigung des tödlich endenden reflektorischen Geschehens durch die vorbestehende Erkrankung des Sinus caroticus in Betracht gezogen werden.
(...)
Strafrechtlich ist die Problematik des Reflextodes immer dann angesprochen, wenn die Beurteilung eines Todesfalles nach Strangulation, namentlich nach Würgen oder Drosseln, ansteht (Dettling, J., Schönberg, S., Schwarz, F.: Lehrbuch der gerichtlichen Medizin. Karger, Basel-New York, S. 290 (1951) / Mueller, B.: Gerichtliche Medizin. Kapitel. Tod und Gesundheitsschädigung durch von außen kommende Einwirkungen. Springer, Berlin-Heidelberg-New York, 2. Aufl. (1975)). Hier stellt sich regelmäßig die Frage nach der Möglichkeit eines Karotissinus-Reflextodes nach einmaliger Gewalteinwirkung gegen den Hals. Entscheidend sind hierbei - abgesehen von den Läsionen der Karotissinus-Region - weitere Leichenbefunde, insbesondere Stauungsblutungen als Ausdruck einer länger dauernden Halskompression. Über deren Entstehung und diagnostische Relevanz hat sich u.a. Pollak (Pollak, St., Mortinger, H., Meisinger, V., Harmuth, P.: Elektrophoretische Untersuchungen zur Blasenbildung am Zwischenstreifen von Strangmarken. Beitr. gerichtl. Med. 44, 535-542 (1986)) geäußert. Nach Bschor (Bschor, F.: Beurteilung von Stauungsblutaustritten im Kopfbereich bei Strangulation und anderen Todesursachen. Beitr. gerichtl. Med. 25, 146-152 (1969)) sowie Camps und Hunt (CH59) treten sie frühestens 10-20 Sekunden nach Strangulationsbeginn auf. Fehlen sie, und zeigen die Halsweichteile nur verhältnismäßig geringe Blutaustritte, so muß beim Vorliegen von Verletzungen reflektogener Zonen die Möglichkeit eines Karotissinus-Reflextodes in Betracht gezogen werden. Sind jedoch reichlich Stauungsblutungen an Kopf und Hals vorhanden, so kann ein Reflextod zuverlässig ausgeschlossen werden. Es bleibt jedoch die Frage, inwieweit zusätzliche reflektorische Einflüsse bei der Strangulation die Überlebenszeit verkürzen können.

(SMZ89, translation KP / Calvin Scott)


Vanezis 1989

Manual strangulation should for all practical purposes be regarded as homicidal. One must be careful to differentiate strangulation from deaths that occur instantaneously after a 'momentary' touch or slight 'unintentional' grip. By definition strangulation implies constriction of the neck to obstruct the airway and/or blood vessels rather than stimulation of the carotid sinus per se.
(...)
The effect of manual compression in a person who has not died virtually instantaneously, as can occur with pressure on the carotid sinus, is to leave bruising in underlying musculature and, frequently, fractures to the larynx and hyoid bone.

This is all Vanezis says about these "deaths that occur instantaneously" in his otherwise rather detailed book on "The pathology of neck injury".


Innala and Ernulf 1989

Another danger is stimulation of the carotid sinus which can cause a drop in blood pressure and sudden heart arrest (RE82). A rope pressure of 10 lb. may be enough to stimulate the carotid sinus to make the heart stop (LR+85).

In LR+85 nothing of the sort is mentioned; this must be a misunderstanding.


Henßge 1990

Die ständige Änderung des von außen auf den Hals einwirkenden Drucks ist für die reflektorischen Folgen auf das Herz von wesentlicher Bedeutung. Ob die Gewalt zu einer Erhöhung der Impulsrate der Pressorezeptoren führt oder aber zu einer Erniedrigung, hängt außerdem vom Ort der Gewalteinwirkung ab: Druckimpuls auf den Karotissinus ist gefolgt von Bradykardie und Hypotonie, Druckabfall durch Kompression unterhalb des Karotissinus von Hypertonie und Tachykardie. Die erhöhte Empfindlichkeit der Pressorezeptoren des Karotissinus gegenüber Dehnung (z.B. bei Zerrung des Halses) im Zustand der Druckentlastung infolge Obstruktion der Karotiden unterhalb des Sinus ist im Tierexperiment nachgewiesen worden (Hering E (1927), Die Karotissinusreflexe auf Herz und Gefäße).
Ob ein Herzstillstand eintritt und wie lange er anhält, hängt u.a. von dispositionellen Faktoren ab (z.B. Syndrom des überempfindlichen Karotissinus, Koronarsklerose, physische Anstrengung). Neben der Störung der Pressorezeptoren kann Gewalteinwirkung gegen den Hals auch zu anderen Vagusirritationen führen. Hier sind die Stimulation der Chemorezeptoren der Karotiden während apnoischer Episoden, die Stimulation von Rezeptoren der oberen Atemwege und die Stimulation fazialer Trigeminusrezeptoren zu nennen. Für das reflektorische Zustandekommen von Bradykardie und Herzstillstand (Fassbender HG (1956), Vagustod und subendocardiale Blutungen. Verh Dtsch Ges Pathol 39: 373-375 / Olb63) wird das Zusammentreffen verschiedener reflektorischer Mechanismen betont (De Burgh Daly MD, Angell-James JE, Elsner R (1979) Role of carotid-body chemoreceptors and their reflex interactions in bradycardia and cardiac arrest. Lancet I: 764-767).
Diese pathophysiologischen Effekte können bei dem dynamischen Geschehensablauf von Gewalteinwirkungen gegen den Hals durch den Abwehrkampf des Opfers keineswegs außer acht gelassen werden. Das Problem kann nicht auf die Standardfrage reduziert werden, ob ein eher beiläufiger Griff zum Hals den Reflextod herbeiführen könne. Vagusvermittelte reflektorische Abläufe können der gewaltsamen Auseinandersetzung zwischen Täter und Opfer in jedem Moment eine richtungsweisende Änderung geben. Das Problem einer Beteiligung des vegetativen Nervensystems am deletären Ausgang komprimierender Gewalteinwirkungen gegen den Hals kann im übrigen auch nicht auf ein isoliertes vagus-reflektorisches Geschehen beschränkt werden: Nach Tierexperimenten kann die gleichzeitige Stimulation von N. accelerans und N. vagus für Kammerflimmern disponierend sein. Mit der gleichzeitigen sympathischen Aktivierung des Opfers durch die Streßsituation ist bei Gewalteinwirkungen gegen den Hals vorn vornherein eine derartige Konstellation gegeben. Funktionsverlust der Hirnrinde und die noch differenzierter zu besprechende "posthypoxidotische Reizphase" sind ebenfalls durch eine gesteigerte Erregbarkeit der Vaguszentren und zugleich sympathische Stimulation gekennzeichnet und für Herzstillstand bzw. Herzkammerflimmern disponierend. Diese Faktoren sind keine individuellen Besonderheiten, sondern potentieller Bestandteil von Gewalteinwirkungen gegen den Hals, insbesondere mit Folge von Bewußtseinsverlust. Sie können auch nach dem Ende einer Gewalteinwirkung gegen den Hals, die zunächst nicht zu irreversibler Hirnschädigung geführt hat, wirksam werden. Das sind Gesichtspunkte, die z.B. bei der Interpretation der Lebensgefährlichkeit eingelassener kürzerer Gewalteinwirkungen gegen den Hals zu bedenken sind.
(Hen90)


Denk, Püschel and Missliwetz 1990

Wiederholt diskutiert, u.E. jedoch bezüglich des tödlichen Ausgangs bisher nicht objektiviert, wurde auch eine Reizung (bzw. Entlastung?) der Karotissinusrezeptoren mit dadurch bedingter Beeinflussung der Herz-Kreislauf-Tätigkeit (Cre83, Hil87, Koi87, RE82).
(...)
Reflex mechanisms leading to death due to stimulation of the carotid sinus appear to be of a merely theoretical nature.
(DPM90, translation KP)


Maxeiner and Dietz 1990

A literature search in the field of sports medicine (...) did not yield one single case of a fatality occurring during the practice of a martial discipline which could be identified as a result of the vagus reflex or the stimulation of the carotid-sinus. Such occurrences are thus at least extremely rare. We are of the opinion that the risk of sudden death of natural cause during the practice of such a sport as judo is much greater than the risk of death resulting from obstructive asphyxiation.
(MD90


Kleemann, Urban, Graf and Tröger 1990

Although a hypersensitive carotid sinus constitutes a pre-condition for carotid sinus syndrome, this does not necessarily mean that individuals with hypersensitive carotid sinus are actually susceptible to the syndrome. Investigations carried out by various authors (...) have shown that the carotid-sinus reflex becomes more sensitive after the age of 35 and that asystole caused by pressure applied to the carotid sinus are more likely to occur at 60 years and thereafter; during the course of these authors' investigations, which involved conducting pressure experiments on approx. 8000 individuals between 15 and 95 years of age, there was not one single fatality that may have occurred as a consequence of pressure simulation applied to the carotid-sinus, even though some at risk patients did participate in the experiment. Drawing on the results of his pressure testing experiments on 3507 individuals, of whom 9% were found to have hyper-active sinus reflexes, Franke (1963) comments that from the age of 40 the pathological responsiveness of the carotid-sinus reflex increases in proportion with increasing age. Arteriosclerosis is assumed to be the reason for this connection with ageing.
(...)
In clinical literature only few fatal complications of carotid sinus stimulation tests are recorded, although this test was and is employed frequently. In most cases at autopsy vascular complications - thromboses of the carotids or the brain stem vessels - were found (Calverley JR, Millikan CH (1961) Complications of carotid manipulation. Neurology 11: 185-189 / Nelson DA, Mahru MM (1963) Death following digital carotid artery occlusion. Arch Neurol 8: 640-643). Only a few cases report fatal ventricular fibrillation during the stimulation test. All of these patients were terminally ill with preexisting cardiac arrhythmia and were treated with digitalis. (GD62 / Hilal H, Massumi R (1966) Fatal ventricular fibrillation after carotid-sinus stimulation. N Engl J Med 275: 175-158 / Alexander S, Ping WC (1966) Fatal ventricular fibrillation during carotid sinus stimulation. Am J Cardiol 18: 289-291) Only in one of these cases an autopsy was done (Alexander u. Ping 1966), which in our opinion is a prerequisite for the conclusion of a reflex death. Without an obduction such an assumption has to remain pure speculation. (...)
Apart from this case (Alexander u. Ping 1966) in clinical literature no further sufficiently documented cases have been reported that justify the assumption of a reflex death.
Neither are there reports on carotid sinus reflex fatalities in sports medical literature (McLatchie GR, Davies JE, Caulley JH (1980) Injuries in karate - A case for medical control. J Trauma 20: 956-958 / Whiteson AL (1981) Injuries in professional boxing. Their treatment and prevention. Practitionier 225: 1053-1057), even though in martial arts significant violence to this region is common. In Judo, for example, the strongest choke holds are applied to the lateral neck regions, sometimes to unconsciousness. (DM88).
Several authors experimented with animals, including Esser (Ess33), Mueller (Mueller B (1960) Tierexperimentelle Studien über den Erstickungstod, insbesondere über Erdrosseln und Erwürgen. Dtsch Z Gesamte Gerichtl Med 51: 377-383) and Credner (Credner C (1971) Das Verhalten des efferenten parasympathischen und sympathischen Reflexanteils bei Carotissinus-Belastung. Dissertation, Universität Göttingen). None of them had any success in killing laboratory animals by percutaneous mechanical or temperature stimulation of the Sinus caroticus.
Neither does the casuistry that has been hitherto described in forensic literature appear convincing: some cases are merely mentioned without any details or autopsy results (Str08 / Sim49 / Walcher K (1950) Leitfaden der gerichtlichen Medizin. Urban & Schwarzenberg, München Berlin / Mueller B (1953) Gerichtliche Medizin 1. Springer, Berlin Heidelberg New York / Bow62Olb63). A review can be found in Kaiser (Kai67). Some of the cases Kaiser lists, however, are certainly not reflex deaths. An example is the case quoted from Strassmann (Str08) where at autopsy bruising on the neck, bloody foam in the airways, a fracture of the left thyroid horn and edema of the lung were found.
The "von Dielingen" case in which the possibility of carotid sinus reflex death was discussed for the first time in forensic literature (Loc30, Gie30) does not qualify as a precedent either. Dyrenfurth and Steinbiß (DS30) and Esser (Ess33) criticized - with justification, we think - that the autopsy results were insufficiently documented and additional histological tests had not been performed.
From today's point of view, an examination of the carotid arteries would be required, as proposed by Sigrist et al. (SMZ89), and an examination of the larynx, as described by Maxeiner and Dietz (MD86).
The casuistry presented by Schollmeyer (Schollmeyer W (1961) Führte eine Blutung im Paraganglion caroticum den Tod herbei? Dtsch Z Gesamte Gerichtl Med 51: 190-193) and Sigrist et al. (SMZ89) describe severe violence to the neck with significant traumatic effects in the carotid area that lead to splits and haemorrhages, in one case even to a rupture of the A. Carotis. Thus, they can not be classified as classical examples of carotid sinus reflex death withouth concrete morphological changes as discussed here. Die Autoren vermuten, daß es bei solchen Verletzungen der Karotissinuswand zur andauernden Reizung der Rezeptoren mit dadurch bedingtem Herzstillstand kommt. Bei einem kurzen Griff an den Hals wird die Herztätigkeit, wenn überhaupt, jedoch nur solange gedrosselt, wie der Druck andauert. Gegen einen endgültigen Herzstillstand durch Druck oder Zug an den Karotiden spricht auch die Beobachtung von Miloslavich (Miloslavich E (1919) Zur Lehre vom Erhängungstode. Vierteljahresschr Gerichtl Med 58: 162-268) bei 2 Justifizierungen, bei denen "im Momente der straffen Zusammenziehung der Schlinge, also im Augenblicke der festen Strangulation ein plötzlicher Stillstand des Herzens und der Atmung erfolgte. Die Herztätigkeit setzte jedoch nach 67 bzw 86 s wieder ein, obwohl die Strangulation bis zum endgültigen Tod weiterbestand. Die Obduktion in diesen und anderen Fällen zeigte keine Risse in der Karotisinterna.
(...)
In an actual case, i.e. after pressure is applied to the neck for a short time without apparent injury or petechiae, how is one to answer questions relating to any perceived threat to life? We believe that none of the casuistry which has hitherto characterised the literature on this subject is suitable for the purpose of substantiating with incontestable certainty (necessary for reaching a criminal verdict) the possibility of death occurring as a result of fatal over-stimulation (ie. pressure applied to the neck) of the carotid sinus reflex. It is therefore highly likely, if not absolutely certain, that such considerations will be ruled out anyway in the case of individuals who do not show any predisposition for a hyperactive carotid sinus reflex as discussed earlier. Even in the case of individuals who do demonstrate such a pre-disposition, the probability of death resulting from the carotid sinus reflex remains extremely remote.
(KU+90, translation KP / Calvin Scott)


Diamond, Innala and Ernulf 1990

Most critical is the physiological reflex that might be brought about with stimulation of the carotid sinus by a sudden compression or pressure surge. This can cause a rapid drop in blood pressure or bradycardia with sudden cardiac arrest, or unconsciousness within 10 seconds. (...) Warnings of danger are in order particularly about the carotid.
(DIE90)

Another example for a popular misunderstanding in the scientific literature.


Shepherd 1990

Compression of the neck may result in death from neural (vagal stimulation or carotid sinus pressure) or obstructive (vascular obstruction or airway occlusion) effects or a combination of the two. The neural effects may result in rapid death and, acting alone, are not associated with significant congestion or with petechial haemorrhages.
(She90)

No references for these statements are given.


Schwerd 1992

Gripping the neck can lead to lethal reflex cardiac arrest via stimulation of the carotid sinus or N. vagus. When arteriosclerotic changes to the arteries are present, the sensitivity of the carotid sinus appears to be increased.
In reflex death, asphyxial signs and sometimes even external trauma in the skin and the structures of the neck are absent.
(Sch92, translation KP)


Spitz 1993

In the celebrated Preppy Murder trial in New York in 1987, the defense argued that the death of Jennifer Levin was caused when Robert Chambers applied a choke hold from behind, tightened the crock of his arm around her neck and flipped her over his head, as she was sitting on his chest, facing his feet. The defense further contended that bruises and abrasions in the front of her neck were caused by creases of Chambers' sleeve and death was instantaneous, unpredictable and accidental, as a result of carotid sinus stimulation.
Had the defense's theory been correct, the pattern of injury of Ms. Levin's neck would have been one of parallel, vertical bruises and abrasions, rather than a double imprint of crossover and X-shaped marks depicting the outline of her own embroidery edged blouse and fingernail scratches on both sides of her neck, suggesting attempted self-defense. The unequivocal pattern of injuries on Ms. Levin's neck indicated that she was strangled by twisting of her own blouse while facing her assailant. This evidence, and the fact that a constriction of the neck would have to be maintained for some time to cause brain death by oxygen deprivation, led to the realization that the death was neither unintentional nor unexpected and to Chamber's conviction.
(...)
In older people with advanced arteriosclerosis of the carotid arteries and in rare instances of hypersensitivity of the carotid sinus, a fall or blow on the side of the neck may cause fainting and even cardiac arrest.
Defense attorneys often argue that the death of the victim was unpredictable, without malice or foresight on the part of their client and consequently accidental, in cases of obvious manual strangulation. The following must be considered in determining whether a death may have been caused by carotid sinus reflex:

  1. Deaths as a result of carotid sinus reflex are highly infrequent.
  2. The victim is likely to be elderly with arteriosclerosis involving the carotid arteries.
  3. The victim was known to be susceptible to carotid sinus stimulation with manifestations of dizziness, headaches, weakness and fainting associated with pressure on either side of the neck.
  4. The presence of injuries, especially fingernail marks (whether the victim's or the assailant's) on the skin of the neck, usually rules out death by carotid sinus stimulation.
  5. Injuries in the soft tissues under the skin should be limited to the areas of the carotid sinus.
  6. Absence of petechial hemorrhages in the conjunctivae and internal organs.

Interestingly, no death due to carotid sinus reflex as a result of attempted self-strangulation has as yet been reported.
Since Brouardel (1896) the term carotid sinus reflex has permeated the forensic literature and served as argument in the defense of strangulation. Yet, it remains a mystery of how a claim of death due to carotid sinus reflex might be applicable to cases of obvious strangulation (Preppy Murder trial).
Many, in fact probably most, cases of strangulation in women are sex related, and I have often heard the defense argue in cases of outright manual strangulation that the death was unexpected during amorous foreplay and was without any intent whatsoever to cause harm.
No doubt sudden cardiac arrest elicited by a carotid sinus reflex is a serious and valuable defense tool. However, such argument appears persuasive only at face value. A closer view of the autopsy findings and frequency of occurrence of carotid sinus reflex indicate the contrary.
(Spi93)


Elfawal and Awad 1994

Death is often neural (vagal stimulation or carotid sinus pressure), or obstructive (airways or vascular occlusion), or a combination of the two (She90). The neural effects may result in rapid death, and if acting alone, may not show classical asphyxial changes (congestion and petechial haemorrhages).
(EA94)


Anscombe and Knight 1996

The other - and to us, most persuasive - explanation, was a period of reflex cardiac arrest caused by transient manual pressure upon the baro-receptors in the carotid sinuses and carotid sheaths. This can trigger afferent stimuli via the glosso-pharyngeal nerves to the brain stem and reflex cardio-inhibitory impulses via the tenth cranial nerve nucleus and vagus nerves. Profound bradycardia on neck stimulation is very familiar to clinicians. It is well-known that this is a common mechanism of death in pressure on the neck in strangulation and hanging. Where there is a pale face, with no congestive/petechial signs, reflex cardiac arrest must surely be accepted as the likely mechanism - though some pathologists attribute death in such cases to cerebral hypoxia due to carotid occlusion.
Even where congestive/petechial signs are present, generally taken to indicate survival for a minimum of 15-30 s, it can never be excluded that subsequent reflex cardiac arrest did not occur further down the time scale, from carotid sinus stimulation by shifting fingers or tightening of a ligature.
(...)
Sudden cardiac arrest from pressure on the neck is well-known, going back to the time of soldiers in classical Greece.
Both Simpson (TS65) and Polson (PGK85) record women dropping dead on the dance floor following a 'playful tweak' of the neck by their partners - and some unarmed combat techniques, such as the 'commando punch' to the side of the neck must also depend upon carotid sinus overstimulation.
(AK96)

Simpson and Polson do not record "women" and their "partners", they both mention one such case in anecdotal form: the notorious "soldier on leave" again.


Knight 1996

Pressure on the baroreceptors situated in the carotid sinuses, the carotid sheaths and the carotid body, can result in bradycardia (slowing of the heart), or in total cardiac arrest. (...) It is often claimed, admittedly without much concrete evidence, that fear, apprehension, struggling and possibly the effect of drugs such as alcohol, may heighten the sensitivity of this vagal mechanism. The release of catecholamines during such adrenal responses may well sensitise the myocardium to such neurogenic stimulation.
The vagal reflex has profound implications in relation to pressure or blows on the neck. Sometimes called 'vagal inhibition', 'vasovagal shock' or 'reflex cardiac arrest', the rapid onset of heart stoppage may antedate any evidence of congestive or 'asphyxial' signs, causing death immediately or within seconds, or at any time thereafter.
It is a matter of some dispute as to whether this reflex can cause immediate cardiac arrest or whether there has to be a period of marked slowing of the heart with negligible cardiac output - or whether an arrythmia such as ventricular fibrillation precedes such an arrest. Probably any combination can occur, but it is an indisputable fact that collapse and apparent death can occur immediately on the application of pressure to the neck.

Is it indeed? If so, there should be at least a few cases to document it.

Overstimulation of nerve endings in the carotid sinus or adjacent arterial sheath may be brought about by direct pressure from fingers, or from a ligature during strangulation or hanging - or from a blow directed at the side of the neck. Severe pain, such as a blow on the larynx or genitals may also trigger a 'vagal response'.
Though different authors vary in the proportion of such deaths that they attribute to reflex cardiac arrest, they all admit to the existence of such a mechanism.

Probably because they all copy from one another, as we have seen.

In the author's own series of fatal pressure on the neck from a variety of causes, the 'classical signs', denoting vascular and perhaps sometimes airway obstruction, were present in slightly less than half the cases. The remaining deaths presented with an absence of congestion, cyanosis and petechiae, the pale faces indicating that cardiac arrest had taken place before the congestive signs had time to appear.

Knight appears to be the only one to ever have attributed such a high percentage of cases to "rapid death from cardiac arrest". What's more, he never published the details on even a single one of them - which he should have done, since no other pathologist seems to have published such a case yet, and it surely would be viewed as most interesting.

One aspect which is uncertain - and virtually incapable of experimental proof in humans - is whether vagus-mediated cardiac arrest can be spontaneously reversible. Where an arrhythmia leads to arrest, resuscitation by cardiac massage or direct current electrostimulation has an excellent chance of revival - though in most forensic situations, such assistance is often lacking or too late.
However, it is not known whether cardiac arrest caused by the vasovagal reflex, can spontaneously revert to normal rhythm some minutes later - or whether it inevitably leads to death if no timely resuscitation is offered.
This may have forensic relevance, as the author has been involved in several cases where pressure on the neck has lead to a comatose, but heart-beating victim, who later dies on artificial ventilation from irreversible brain damage. In the absence of medical data, the problem then arises as to whether the brain damage was caused by prolonged carotid artery occlusion from neck pressure - or was the result of a momentary neck pressure which caused reflex cardiac arrest, with spontaneous reversion to normal rhythm more than five minutes later, by which time irreversible cerebral damage had occurred.

This has been investigated by several authors. E.g., MD90 state that in such cases obstructive asphyxia had been uphold for at least several minutes after the victims lost consciousness. There is no documented case of someone sustaining cerebral damage after short and nontraumatic pressure on the neck. If the author "has been involved in several cases", maybe he should have published one of them.

This phenomenon has considerable legal as well as medical significance, as sudden death from 'vagal inhibition' can occur with total unexpectedness even with relatively slight pressure to the neck. Keith Simpson (Sim85) and Polson (no source given) recorded cases many years ago in which a soldier at a dance playfully 'tweaked' his partner's neck and was mortified to see her drop lifeless to the floor. Many such cases are on record and every forensic pathologist of any experience has examples in his own records.

Simpson and Polson seem to mention one single case (even if their descriptions differ somewhat), and they certainly did not "record" it. There are no "many such cases" on record anywhere (on the contrary: the lack of such cases is mentioned more than once), and if "every forensic pathologist of any experience has examples in his own records", it is quite remarkable that not one of them has yet thought of publishing them.

Where it can be shown that the death occurred rapidly and without prolonged manual gripping of the neck, the defence may be raised that neither death nor serious injury was contemplated by the accused. It would be much harder to establish this lack of intent if the grip was maintained long enough to lead to florid congestion and petechiae in the face.

It is important to remember that the cardiac arrest mode of death may be mixed with the congestive-petechial mode in that, though the first stages of pressure may continue for long enough for congestive-asphyxial signs to appear (perhaps a minimum of 15-30 seconds), a change in grip may then allow the fingers to impinge on the carotid structures and lead to reflex cardiac arrest. Thus the progression of the pure 'asphyxial' progress may be abruptly terminated at any point along its pathway to death by the superimposition of 'vagal inhibition', so that the intensity of the congestive changes may be of any degree in any given death.
The duration for which pressure must be maintained is often a contentious issue in criminal trials, as the 'inadvertent squeeze' which causes rapid vasovagal cardiac arrest is likely to be viewed as less culpable than a prolonged, unremitting gripping of the throat.
It is virtually impossible to measure the average minimum time of gripping that will produce congestion, cyanosis and petechiae from venous occlusion. As so often is the case in forensic medicine, animal experiments are useless for this purpose and obviously few cases of strangulation homicide are ever reliably witnessed, especially by some dispassionate observer with a stopwatch! Even in non-fatal cases - which incidentally, can produce far more florid examples of facial and eye haemorrhages than deaths - there is almost never any independent, accurate measurement of the time for which the neck was compressed.
It has been arbitrarily suggested that 15-30 seconds is probably the minimum period which will give rise to petechiae in the eyelids, conjunctivae and facial skin, but this really is 'picking a figure from the air', with little scientific justification.
Some years ago, the British Home Office and the Royal College of Pathologists set up a small working party to study this problem, composed of several experienced forensic pathologists and a respiratory physiologist - but the project was soon abandoned because of a total lack of reliable data.
Though it is easy to demonstrate that facial congestion develops within a few seconds of total jugular occlusion, petechiae - the only lasting sign after the venous return is re-opened - do not appear as quickly from neck pressure. However, they can occur from sudden, transient rises in venous pressure, such as sneezing or coughing - whooping-cough is a well-known example - and during the Valsalva experiment of forcibly trying to expire against a closed glottis. Eye petechiae and retinal haemorrhages can also occur during the chest compression of energetic cardiac massage during resuscitation.

Vagal inhibition of the heart from stimulation of the carotid neural complex may occur in any form of pressure on the neck, but is much more common in manual strangulation than with a ligature, hanging excepted. Fingers seem more prone to dig deeply and find the structures under the anterior edge of the sternomastoid muscle. Perhaps the movements of the fingers, expecially during the shifting postures of a struggle, more readily impinge upon the carotid bifurcation than the more static position of a ligature.
The majority of hangings, however, present with a pale face, free from congestive-haemorrhagic signs.
This seems to be caused by the more precipitate impact of the noose on the carotid structures when the victim's weigh abruptly bears down, though Polson favoured actual carotid occlusion and hence cerebral ischaemia as the common cause of death in hanging. The scarcity of carotid intimal damage in suicidal hangings does not favour this view.
(...)
Another cause for sudden cardiac arrest is a blow to the neck or throat. This is the basis of the so-called 'commando punch' and some of the oriental martial arts also contain this in their repertoire - often forbidden because of its potential lethality. The edge of the hand is brought forcibly across the side of the neck or the front of the larynx.
Direct violence to the carotid region naturally causes gross stimulation of the afferent nerve endings. Blows directly to the larynx indirectly stimulate the sinus region or the laryngeal sensory nerve endings may themselves trigger the cardio-inhibitory reflex.
It is well known that the hypopharynx and larynx are particularly sensitive to stimulation, which accounts for the sudden deaths from impaction of food in the larynx, or from the flooding with cold water that causes some sudden immersion deaths. The testicles and uterine cervix also have a similar reputation for leading to sudden cardiac death, if unexpectedly overstimulated, especially when the myocardium is pre-sensitised by catecholamines released by fear or emotion.
(...)
Death is, however, more often caused by reflex cardiac arrest from pressure on the carotid structures. Many more victims of hanging are found to have pale faces, rather than the congested, haemorrhagic appearance of the slower asphyxial type of death. James and Silcocks, in a 15-year survey of hangings in Cardiff, found congestive-petechial features in 27 per cent, being related to the completeness of suspension.
Polson suggested that the usual pale face in hanging is caused by cerebral ischaemia from bilateral occlusion of the carotid arteries rather than a vasovagal effect, though this seems incapable of proof. In either event, the death can be taken to be rapid if no asphyxial signs are present.6
(Kni96)

The diagnosis of carotid sinus reflex death can not be used to explain any death from reasons unclear. While the presence of congestive/petechial signs means with some certainty that no carotid sinus reflex death has taken place, one can not simply conclude that in their absence a carotid sinus reflex death must have been the cause of death. Several other authors have noted that in hanging frequently no "congestive, cyanotic nor haemorrhagic stigmata" may be found without ascribing this to reflex mechanisms. Examples:

Typical findings - which, unfortunately, are frequently absent even in undoubted asphyxia - are (...)
(Kni76)

The face of the victim is usually pale or of leaden hue. (...)
Petechial haemorrhages, as in any other asphyxial death, may be present in the skin of the face and forehead and beneath the conjunctivae. They are, however, infrequent, being absent in nine out of every ten victims; they are normally present when hanging has been from a low point.
(PGK85)

However, it should be appreciated that in the majority of hangings the face appears normal or pale; the ligature mark, and, frequently, protrusion of the tongue are the only external signs of hanging.
(Van89)

Due to the specific mechanism of death (sudden ischemia of the brain) in typical hangings neither external nor internal signs of asphyxia can be found.
(Sch92)

Complete interruption of blood flow to the brain, as when the feet are off the ground, causes the face to be pale. Neither swelling nor pinpoint hemorrhages are noted above the noose.
(Spi93)

I can't see why Polson's theory should be more "incapable of proof" than Knight's own. The relation between completeness of suspension and lack of congestive-petechial features has been noted not only by James and Silcocks, but other authors as well (LR+85, Sim88). If the underlying reason was a reflex mechanism, wouldn't the pale face be apparent in just as many incomplete suspensions?


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