Mechanical compression with blood vessels in the neck causes a reduction in oxygenation of the brain, leading to cerebral hypoxia/ischaemia, anaerobic metabolism, and acidaemia/acidosis (similar to the effects of cardiac arrest on the brain (Longstreth 2001).

The term “asphyxia” is commonly used in the forensic literature to describe this sequence, but it is not a term used in clinical practice, except in relation to “birth asphyxia”, a situation that has also been criticised (Depp 1995).

The term “asphyxia” - literally meaning without a pulse - should be avoided, according to the Goudge Inquiry (Goudge 2008), as it is too unspecific a term. 

Alternative mechanisms of death following pressure to the neck include some form of neurologically-mediated cardiac arrest, stimulated by mechanical compression of neck structures such as the carotid sinus, and carotid body.


Test your anatomy of the respiratory tract by labelling the structures here ...

And interact with a 3D anatomy model of the neck here ...


pathophysiology of hanging


Suicide by hanging. Atlas of Legal Medicine (Eduard Ritter Von Hoffmann 1989)

Source: National Library of Medicine


Despite hanging being a common form of suicide, the precise pathophysiological mechanism(s) involved is (are) poorly understood.

Historically, pathophysiological mechanisms thought to be involved included (Clement et al 2010):

  • respiratory asphyxia,
  • occlusion of blood vessels in the neck causing an interruption of cerebral blood flow, and
  • cardiac inhibition secondary to nerve stimulation.

The Working Group on Human Asphyxiation (WGHA), formed in 2006, has carried out reviews of the literature regarding pathophysiological mechanism theories, the results obtained from animal experiments (and a consideration of their applicability to determining the mechanism of death in humans) and has reviewed filmed suicidal/ accidental hangings in order to describe the sequence of events in such hangings.

A review of data from animal studies (Boghossian et al 2010) - of which the rat is perhaps the best model due to anatomical considerations - revealed (in general):

  • muscular movements ceased after 1-3.5 mins (with early tonic-clonic convulsions being described),
  • complete circulatory collapse occurs between 4-8.5 mins, and
  • cessation of cerebral blood flow, rather than airway obstruction, seems to be the principal cause of respiratory decline.

In a review of filmed hangings (Sauvageau et al 2010), the following general observations were made by the WGHA:

  • rapid loss of consciousness (at 8-18 seconds),
  • convulsions (at 10-19 seconds),
  • decerebrate and decorticate rigidity,
  • loss of muscle tone (between 1 min 38 seconds and 2 mins 15 seconds),
  • isolated body movements 'from time to time' (last between 1 min 2 seconds and 7 mins 31 seconds),
  • deep rhythmic abdominal respiratory movements (last between 1 min 2 seconds and 2 mins 5 seconds).

hanging in history - China


[The corpse] was suspended from the cross-beam of the north wall within the eastern bedroom of the house facing south, by a hempen rope as thick as one's thumb. The noose was tied round the neck, and knotted at the nape; above it the rope was twice looped around the cross-beam and then tied in a knot, leaving a tail end some two feet long. The top of the head was two feet under the cross-beam, and the feet were suspended two inches above the floor. The head and back touched the wall, and the tongue protruded slightly; below, excreted faeces and urine had soiled both his legs. Upon releasing the rope, the breath issued with a gasp from the mouth and the nose. The rope left a compression bruise mark (around the neck) except for a two inch space at the nape. Elsewhere the body showed no signs of knife-blade wounds or traces of (damage by) wooden (cudgel) or rope. The cross-beam was one span in circumference, three feet long, and projected westwards two feet beyond the edge of an earthen platform (on the ground). From the top of this it was possible (for the deceased) to lead and bring together the rope around the beam.

'Death by hanging' in 'Models for Sealing and Investigating (Feng chen shih)'. Found written on bamboo slips in a tomb at Shui-hu-ti near Yun-meng in Hupei,  China in 1975, and estimated to date between 266 and 246 BC.

'A history of forensic medicine in China', Gwei-Djen L, Needham J, Medical History 1988; 32:357-400

petechial haemorrhages


Compression of jugular veins, with unimpeded arterial flow, results in raised intravascular pressure in the head, and facial congestion.

Petechiae - small areas of vascular bleeding of a few millimeters in size - form at the level of the pre-capillary arteriole (Humble 1949) in conjunctivae, mucus membranes, and the skin of the face and eyelids, due to mechanical disruption of vessel walls (Ely and Hirsch 2000, and Lasczkowski 2005).

Ely and Hirsch (2000) found no causal link between the formation of petechiae and hypoxia/asphyxia ; petechiae are formed in proportion to the degree of venous obstruction.

Purdue (2000) considers subconjunctival haemorrhage as implying a greater degree of force applied to the neck than is required to produce petechiae.

There is no relation between petechiae and alcohol and drug use (Rao & Wetli 1988). 


Time needed to cause petechiae?

  • Fifteen to thirty seconds (Anscombe and Knight 1996)
  • Ten to thirty seconds (Plattner et al 2005)
  • Fifteen seconds maximum (Copley & Kozam 1951) – using the capillary fragility test
  • “Shortly after” gravity inversion in healthy individuals (Friberg & Weinreb 1985)


Petechiae seen in context other than mechanical compression:

  • Cardiac deaths.
  • Electrocution (not related to voltage or currents); possibly due to raised blood pressure from contractions and cardiac arrests (Karger et al 2002)
  • Post-mortem artefact from prone position
  • Head trauma
  • Trauma with subsequent resuscitation
  • Epileptic seizures (but elements of positional asphyxia may be relevant)
  • Paroxysms of sneezing and coughing
  • Sepsis
  • Childbirth, vomiting, Valsalva manoeuvre
  • Gravity inversion


Petechiae are also seen in cases of arm chokeholds i.e. Shime-waza (a judo hold designed to bring about loss of consciousness in ten seconds).  In the carotid sleeper and bar-arm control used in law enforcement has been linked to some deaths, and in these cases petechiae, soft tissue haemorrhage, and laryngeal fractures have also been reported.

In assaults etc., raised venous pressure in the neck veins may also be related to struggling/screaming against obstructed airways, raising cardiac output and blood pressure, and possibly also linked with fragile vasculature, especially in the elderly, giving rise to more petechiae (Ely & Hirsch 2000).

loss of consciousness and pressure to the neck


Swann & Brucer (1949) – dogs survived seven to fourteen minutes of obstructive asphyxiation, and it was shown that there was a raised partial pressure of carbon dioxide, then reduced heart rate, followed by a terminal tachycardia and abrupt cardiac failure.

The pressure required to obstruct various neck vessels has been reported as:

  • Jugular veins (2kg)
  • Carotid arteries (2.5 – 10kg, or 250mmHg), a scenario not normally seen in manual strangulation (Puschel et al 2004)
  • Airways (8 – 12kg)
  • Vertebral arteries (35kg)
  • Loss of consciousness in chokeholds is thought to be at approximately ten seconds
  • Rossen et al 1943 states that loss of consciousness occurs in five to eleven seconds where there has been carotid and vertebral artery compression, whilst Sauvageau and Racette (2007) state that loss of consciousness in hanging occurs at approximately 13 seconds

NB Reay & Holloway (1982) state that during neckholds, the blood flow to the head is reduced by 85% within six seconds.

neck injuries in strangulation


Skin – fingernail abrasions and/or fingertip bruises (Camps & Hunt 1959; Luke 1967).

Soft tissue bruising – manual greater than ligature (Iserson 1984), especially where hands are re-applied; chokeholds; including congestive stasis in salivary glands, and the base of the tongue; soft tissue bruising is seen at the same level as a ligature.

Laryngohyoid complex – said to be frequent (Bux et al 2006); in greater than 50% of cases (Pollanen 2001), “the most consistent morphological marker of homicidal neck compression, especially if the complex is ossified due to increasing age” (Pollanen 2001; Brockholdt et al 2003); injuries in the complex are especially seen in manual strangulation (Green 1973; Harm & Rajs 1981); “pathonomonic of throttling” (Adelson 1974).

other circumstances of laryngohyoid fractures



  • Hanging (in 72.5% in Zatopkova et al 2018; in 68% Nicolic et al 2003; in 67% Betz and Eisenmenger 1996; in 25% James and Silcocks 1992; in 9% Feigin 1999)
  • Falls (Perez et al 1983, Kadish et al 1994), at low level (i.e. agonal falls) according to Bux 2006, and high level falls (De La Grandmaison et al 2006)
  • Direct/indirect trauma – e.g. striking handlebar of bike (Kleinsasser et al 2000), or in motor vehicle collisions/”runovers”

The mechanism of laryngohyoid fracture in such circumstances might be direct pressure against the cervical spine (Adelson 1974), or thyrohyoid ligament traction.  NB artefacts should be excluded.

microscopy and pressure to the neck


  • Lungs – non-specific (Adelson 1974); pulmonary oedema/haemorrhage etc. (Puschel et al 2004).
  • Thyroid cartilage (Rajs & Thiblin 2000) – haemorrhage, retraction of fracture fragments (angulation), invagination of pericondrium +/- rupture, myocyte waviness/contraction band necrosis, “opaque” fibres (swollen myocytes, loss of striations), fibrin, white blood cells.

laryngohyoid fractures, and associated injuries in hanging


  • Petechiae in 25%
  • Soft tissue bruising in 20 – 30%
  • Laryngeal fracture 35 – 45%

Adelson (1974) criteria for a 'valid diagnosis' of manual strangulation


  • Bilateral skin trauma
  • Subjacent soft tissue haemorrhage
  • Laryngeal/hyoid injuries

Without trustworthy features of cervical squeezing, facial and ocular petechiae carry no specific diagnostic weight.

 According to Polson & Gee (1973), the range of injury appearances is “unlimited”. 

homicidal vs suicidal ligature strangulation (Maxeiner & Bockholdt 2003)


  • Homicidal – intensity of local neck injuries; extra cervical injuries pointing to assault; lack of ligature; clear ligature abrasion.
  • Suicidal – marked congestion above the level of the ligature; insignificant neck structure haemorrhage; several turns of the ligature; knot at the front or the sides; absence of clear ligature mark; absence of defence injuries (which are present in 33% of homicides according to Mohanty et al 2007); rarely fractures of laryngohyoid complex.

NB The nature of the ligature marks depends on the roughness of application, and the type of ligature etc. (Camps and Hunt 1959).

Etymology: ligature word origin at Wiktionary

questions to be answered in cases of pressure to the neck (Camps & Hunt 1959)


  • How was it applied? (look at the injuries).
  • Length of application time? (based on “asphyxial signs” and vital reactions; Class 1 cases include well-developed petechiae, conjunctival and pulmonary oedema, and congestion of the root of the tongue, where pressure has “usually been maintained for at least 30 seconds, and probably longer”.  Class 2 cases are those in which there are no petechiae and the face is pale, these cases probably involving rapid “arrest”.
  • Force of application? – considerable violence will be associated with bruising and laryngeal injury, and congested changes in such cases are marked.

degree of force used in manual strangulation?


  • Polson & Gee (1973) – if abundant damage to neck structures, it is reasonable to say “appreciable force” or, occasionally, “considerable force”.
  • If there is a fracture of the larynx or hyoid bone, the person bringing about pressure to the neck must have been aware of doing it, and it scarcely represents an “accidental touch or momentary grip”.

Harold Loughans and the John Barleycorn murder


Rose Robinson was the licensee of the John Barleycorn pub in Portsmouth, who was in the habit of putting the day's takings into handbags that she kept with her at all times. Sometime during the night of 28th-29th November 1943 she was killed; a window had been forced, and her money was gone.

Dr (later Professor) Keith Simpson, a forensic pathologist from Guy's Hospital, London, was asked to attend the scene, and he thought that she had been strangled in the bedroom where her body lay, her murderer kneeling or sitting astride her.

The fingermarks told a clear story: a deep bruise on the right of the voice box, presumably made by a thumb, and three lighter bruises in a line on the other side.... There were no curved fingernail impressions immediately related to these marks, but there were several scratches on the neck that could have been made by Mrs Robinson as she struggled to prise away her attacker's hands.

Harold Loughans was picked up by police in London nearly a month later for trying to sell stolen property. He told them that he was 'wanted for things far more serious than this. The Yard wants me. It's the trapdoor for me now'.

He subsequently told police that he had grabbed Mrs Robinson by the throat with his right hand and killed her. The police were worried though; Loughans 'didn't have any fingers' on his right hand!

Simpson examined the right hand and found that Loughans had finger stumps - he had lost the distal two phalanges of each finger - and an intact thumb.

The hand could still have reached four inches, and the stumps would have had an even greater leverage than fingers of full length. But, of course, if the old lady was lying on the floor he only needed to put the weight of his body behind that hand to strangle her.

At the trial, Loughans denied murder, and said that his confessions had been fabricated by police. Alibi witnesses were produced, and the trial ended with the jury unable to agree a verdict.

The re-trial took place two weeks later, and Simpson's evidence that Loughans could have strangled Mrs Robinson with his deformed hand was questioned; Sir Bernard Spilsbury was called for the defence. He had shaken Loughan's hand at Brixton Prison and been asked to grip it as hard as he could. 'I do not believe he could strangle anyone with that hand', said Sir Bernard. Simpson thought that the 'magic of his reputation was too much for the jury.' Loughans was acquitted.

Loughans was not free for long: waiting police arrested him for another burglary, and he was convicted. Such was his skill with the 'lame' right hand, that he was nicknamed 'Handy' in prison!

In 1963 he sued The People paper for libel; they had published extracts from the autobiography of JD Casswell KC, the prosecution barrister from the Robinson trial, who made it clear that he thought Loughans lucky to have been acquitted of murder.

Loughans had persuaded Francis Camps, another forensic pathologist in London - Spilsbury was, by this time, dead - that he had little strength in his right hand, although testing had shown it to be capable of exerting a grip 'strength' of 14 pounds, and that his grip had recently been much weakened because he suffered from stomach cancer. Loughans was unsuccessful in his civil case, but the story did not end there.

He walked into the offices of The People a few months later and confessed to Mrs Robinson's murder; the newspaper photographed him writing his confession, a pen held in his 'useless' right hand.

I want to say I done that job. I did kill the woman in the public house in Portsmouth.

[See Simpson K. Forty Years of Murder. 1978 chapter 7.]

pressure to the neck and sudden cardiac death


Arteries in the neck

Source: Wikipedia


The application of pressure to the neck can result in death due to asphyxia, but rare instances have been reported of mild or ‘playful’ pressure being applied to the neck that have resulted in ‘instantaneous death’.

Traditionally these ‘freak accidents’ have been ascribed to ‘vagal inhibition’ or ‘reflex cardiac arrest’, involving stimulation of the carotid sinuses.

The carotid sinus is a dilatation of the lower end of the internal carotid artery, and functions as a baroreceptor (a stretch receptor) responding to changes in vessels induced by the arterial pressure (Standring 2005).

Arterial baroreceptors play a key role in short-term blood pressure control. Impulses arising in the sinus travel up afferent fibres in the carotid sinus nerve (a branch of the glossopharyngeal nerve) and on to the nucleus of the tractus solitarius (NTS) in the medulla.

Stimulation of the NTS inhibits sympathetic nerve impulses to peripheral blood vessels (vasodilatation). Stimulation of the vagal nuclei in the medulla brings about a bradycardia, and the combined effect is to reduce heart rate and reduce blood pressure (Berne and Levy 1996).


carotid body anatomy - for full size version see at source

Source: Neuroanatomy at University of British Columbia



The baroreflex is very rapid (<1sec), but is inhibited by stimulation of the hypothalamic defence area in ‘fight or flight’ situations. Central pathways controlling the cardiovascular system are complex, involving the cerebral cortex, hypothalamus and cerebellum as well as the medulla (Sunthareswaran 1998).

In addition, alteration in baroreflex sensitivity has been shown to be linked to an increased risk of the development of Ventricular Fibrillation (VF) in experiments on dogs with healed myocardial infarcts (Schawartz et al 1988).

In clinical medicine, it is known that pressure on the carotid sinus can alter the heart rate, and this principle is exploited to elucidate the underlying mechanism and provide prompt treatment of various supraventricular tachycardias as well as differentiate them from ventricular arrhythmias.



carotid sinus pressure




Carotid sinus pressure (© WIFM)


Carotid Sinus Pressure (CSP) involves the stimulation of the parasympathetic nervous system resulting in reduced heart rate and reduced cardiac workload. Susceptibility to sympathetic induction of myocardial ischaemia and VF should be reduced, but it is possible that carotid sinus hypersensitivity results in excessive parasympathetic stimulation and cardiac standstill.

This procedure has also been shown to induce atrioventricular (AV) block and asynchrony of ventricular muscle excitability with one case report of VT, providing a substrate for electrical heterogeneity and thus the development of fatal arrhythmias.

It is possible that susceptible individuals have unusually rich ventricular cholinergic innervation, or that following the release of CSP there is a reflex catecholamine release from myocardial stores rather than sympathetic nerve endings, allowing asymmetric distribution and genesis of ventricular ectopics and arrhythmias (Cohen 1972).

Deaths from ‘vagal stimulation’ have been reported for many years (Simpson 1949, Hirsch and Adams 1998), where pressure on the neck, blows to the groin or medical procedures have resulted in the instantaneous death of the victim.

The stimulation of sensory nerves of skin, pharynx, glottis, pleura, peritoneum covering viscera etc result in the afferent stimulation of the parasympathetic nervous system, resulting in a fatal arrhythmia. Vagal stimulation has been found to be profibrillatory to atria, but paradoxically to mitigate ventricular arrhythmias (Willich 1993).

Acute stimulation of the CNS by drugs or electrical stimuli lowers the threshold for cardiac electrical instability, and may evoke a variety of arrhythmias including VF, suggesting a role of the higher centres which has not been fully elucidated.

Critical vasomotor regions of the brain include the 3rd ventricle, the midbrain and medulla oblongata. Interruption of sympathetic and parasympathetic pathways between the brain and heart, for example through trauma, can result in instantaneous death (Hirsch and Adams 1998).

More recently, Purdue (2000) has proposed mechanisms for asphyxial deaths, including mechanisms of sudden death during the application of pressure to the neck.

Novel terms are utilised in an attempt to explain the pathophysiological mechanisms involved, which describe a spectrum of insults leading to cardiac dysfunction;

  • Remotely Stimulated Cardiac Dysfunction (RSCD)
  • Cumulative Cardiac Insult (CCI) and
  • Instantaneous Neurogenic Cardiac Arrest (INCA)

Pressure on the neck during, for example manual strangulation would incorporate elements of neural and humoral mechanisms together with hypoxic changes to bring about CCI and death.

It is suggested that prolonged pressure on the carotid arteries below the level of the carotid sinuses could bring about sympathetic discharge, increasing the risk of ectopic beats and VF (particularly in the setting of fear). Pressure above the level of the sinuses (or on them) would result in parasympathetic discharge and potentially asystole in those with sensitive baroreceptors.

Without the elements of asphyxia and prolonged compression, the concept of INCA is proposed, which represents the extreme end of the CCI spectrum, and involves overwhelming parasympathetic discharge from highly sensitive carotid sinuses.

It is also noted that a similar effect may also be induced by the application of force to other vital ‘nerve centres’ such as the solar plexus (at the pit of the stomach), the front and sides of the neck, the philtrum of the upper lip, the inner aspect of the knees, the cervix and the genitalia (especially the testes).


Opponents to the theory of the caotid sinus pressure theory of sudden death during pressure to the neck?

  • DiMaio and DiMaio (1989) – “highly improbable and suspect”.
  • Spitz & Fisher (1993) – “highly infrequent”, persuasive only at face value, and probably only of relevance in the elderly, and those with coronary artery atherosclerosis and/or carotid artery atheroma.

autoerotic asphyxiation - Hazelwood criteria (Shields et al 2005)


  • Physiological mechanism for obtaining/enhancing sexual arousal that is dependent on either a self-rescue mechanism, or the victim’s judgement to discontinue its effect
  • Solo sexual activity
  • Sexual fantasy aids
  • Prior dangerous autoerotic practice
  • No apparent suicidal ideation

positional asphyxia (Bell et al 1992)


  • Finding the victim in a position that doesn’t allow for adequate respiration, including restrictive/confining positions, flexion of the head onto the chest, partial/complete airway obstruction, or neck compression
  • No evidence to implicate another person – the history/scene indicate the victim was responsible for inadvertently placing him or herself in that situation
  • Inability of victim to extricate him or herself e.g. intoxicational dementia for example
  • No evidence of internal airway obstruction e.g. aspirated food
  • No evidence of carbon monoxide or other suffocating gas inhalation
  • No evidence of significant cardiac disease (NB Byard (2008) would say that there may be cardiovascular or respiratory disease that has predisposed to positional asphyxia)

NB Positional asphyxia peaks in infancy/early childhood – from accidents/unsafe sleeping arrangements – and then later in life.

traumatic asphyxia in history - 'Burking'






revise your anatomy


Revise your anatomy of the neck/ larynx with the help of anatomy resources on the web ..

revise your neck muscle anatomy




living lung ipad app



revise your anatomy - features of vertebrae



cervical spine injury




patterns of cervical spine injury - for full details, see the excellent Radiology Assistant.


Classification of 'hangman's fractures' via Radiology Assistant.

  • Type I (65%)
    • hair-line fracture
    • C2-3 disc normal
  • Type II (28%)
    • displaced C2
    • disrupted C2-3 disc
    • ligamentous rupture with instability
    • C3 anterosuperior compression fracture
  • Type III (7%)
    • displaced C2
    • C2-3 Bilateral interfacet dislocation
    • Severe instability


Additional resources on cervical spine trauma evaluation as well as revision resources on cervical spine anatomy, visit this website from the University of Viginia.



anatomy of cervical spine trauma



Capital punishment - judicial hanging in history


Source: Wikimedia Commons





restraint-related deaths/ excited delerium


Dr Nat Cary talks about excited delirium from TBIJ on Vimeo.


But see, his face is black and full of blood,

His eye-balls further out than when he lived,

Staring full ghastly like a strangled man;

His hair uprear'd, his nostrils stretched with struggling;

His hands abroad display'd, as one that grasp'd

And tugg'd for life and was by strength subdued:

Look, on the sheets his hair you see, is sticking;

His well-proportion'd beard made rough and rugged,

Like to the summer's corn by tempest lodged.

It cannot be but he was murder'd here;

The least of all these signs were probable.


The Earl of Warwick describes the murdered body of Duke Humphrey of Gloucester in Henry VI, part 2 - Act 3, scene 2 by William Shakespeare


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