between hypostasis and bruising difficult and eventually impossible. Even histological examination may be of little help when the tissues become markedly degenerate.
physicochemical basis of the phenomenon is discussed, the availability of glycogen and adenosine triphosphate in the muscle is a crucial element in rigor formation. Muscular exertion affects the interaction of these substances and has- tens the onset of rigor. Cadaveric spasm, dealt with later, may well be an extreme variant of this accelerated rigor.
In view of the wide range of times at which the various stages of rigor appear and fade, it is a poor determinant of the time since death, compared with estimations of body tempera- ture. Niderkorn’s early work (1874) on 113 bodies showed a range of 2–13 hours for rigor to be complete, the main clus- ter being from 3 to 6 hours after death, a shorter period than would be accepted now. Mallach (1964) compiled a table from 150 years of published data, which suffered from gross variation in observer methodology (Table 2.3).
The following is a reasonable ‘spot check’ for use in aver- age temperate conditions:
■ If the body feels warmand is flaccid, it has been dead less than 3 hours.
■ If the body feels warmand is stiff, it has been dead from 3 to 8 hours.
■ If the body feels coldand is stiff, it has been dead from 8 to 36 hours.
■ If the body feels coldand is flaccid, it has been dead more than 36 hours.
This crude estimate should never be used as a definitive statement in legal proceedings, as it is only meant as a rough guide ‘on the spot’.
Rigor mortis in other tissues
Rigor occurs in all muscular tissues and organs, as well as the skeletal muscles. The iris is affected so that ante-mortem constriction or dilatation is modified. The rigor may be unequal in each eye, making the pupils unequal, confirming
the fact that the post-mortem position is an unreliable indi- cator of toxic or neurological conditions during life.
In the heart, rigor causes the ventricles to contract, which may be mistaken by the inexperienced pathologist for left ventricular hypertrophy; this can be excluded by measuring the total weight, estimating the relative size of the left side, measuring the ventricular thickness (admittedly a rough guide) and – where the issue is important – by dissection and differential weighing of the two ventricles.
Rigor in the dartos muscle of the scrotum can compress the testes and epididymis which, together with the contrac- tion of muscular fibres in the seminal vesicles and prostate, may lead to post-mortem extrusion of semen from the ureth- ral meatus. This has been wrongly attributed to sexual activity and orgasm just before death in cases where a defence of provocation against a homosexual advance has been put forward. Mant showed that many corpses dying from a variety of causes have seminal fluid either at the meatus or in the penile urethra (Mant 1953, 1967; Mant and Furbank 1957). It is also said, without much foundation, that deaths from hanging and ‘asphyxia’ are commonly associated with post-mortem seminal emission.
Rigor in the erector pili muscles attached to the hair fol- licles can cause a pimpling or ‘goose-flesh’ appearance with elevation of the cutaneous hairs. This may have given rise to the persistent myth that the beard grows after death, though an additional explanation is that post-mortem des- iccation and shrinkage of the skin allows the hair stubble to appear more prominent.
Studies by Krompecher and Bergerioux (1988) have shown that rigor also sets in more quickly in deaths from electrocution – and that it passes off more rapidly.
The biochemistry of rigor mortis
Though this has little direct forensic relevance apart from the association of the early onset of rigor with muscular
Rigor mortis
TABLE2.3 Time course of cadaveric rigidity as stated by previous literature Hours post-mortem
Mean with
Limits of 95.5 per cent
Number of standard
probability (2s) Variations
publications Rigor phase deviation(s) Lower limit Upper limit Lower limit Upper limit evaluated
Delay period 32 – 7 1⁄2 7 26
Re-establishment possible Up to 5 – – 2 8 –
Complete rigidity 81 6 10 2 20 28
Persistence 5714 29 85 24 96 27
Resolution 7632 12 140 24 192 27
exertion, the muscle chemistry of the phenomenon has been studied in great detail.
Szent-Gyorgi (1947) discovered that the essential con- tractile substances in muscle were the two proteins actin and myosin, arranged in interdigitating filaments. They form a loose physicochemical combination called ‘actomyosin’, which is physically shorter than the two substances uncom- bined (Hanson and Huxley 1955). If energy is supplied to the latter pair, the subsequent combination contracts. This energy is obtained by the splitting off of a phosphate com- plex from adenosine triphosphate (ATP) which then becomes adenosine diphosphate (ADP) (Erdos 1943). The free phosphate then engages in a phosphorylation reaction that converts glycogen to lactic acid, high energy being released in the process. Some is used to resynthesize the ATP from ADP, by the donation of a phosphate group from creatine phosphate; the remainder goes to activate the actin–myosin reaction.
In addition to supplying energy, ATP is responsible for the elasticity and plasticity of the muscle. The lactic acid is leached away back into the bloodstream and is returned to the liver for reconversion into glycogen. All these reactions are anaerobic and can continue after death, albeit in a dis- torted form.
In life there is a fairly constant concentration of ATP in the muscular tissues, there being a dynamic balance between utilization and resynthesis. At death, however, the ADP to ATP reaction ceases and the triphosphate is progressively diminished, with lactic acid accumulating.
After a variable period, depending on temperature and the amount of ATP remaining, the actin and myosin become rigidly linked into a rigid, inextensible gel, with consequent stiffening of the muscle (see Bate-Smith and Bendall 1947;
Forster 1964).
The resynthesis of ATP is dependent upon the supply of glycogen, which is depleted by vigorous activity before death;
this explains the rapid onset of rigor in these circumstances.
Normally there appears to be an initial period soon after death when the ATP level is maintained or even increased as a result of phosphate liberation by glycogenolysis.
Rigor is initiated when the ATP concentration falls to 85 per cent of normal, and the rigidity of the muscle is at maximum when the level declines to 15 per cent (see Bate- Smith and Bendall 1949).
Gross effects of rigor mortis
There has been some controversy over whether rigor only stiffens the muscles or actually shortens them. Sommer, as long ago as 1833, claimed that muscles contracted after death and the changes were actually known as ‘Sommer’s movements’. There have always been semi-apocryphal tales
of corpses moving in the mortuary and there seems little doubt that, if a limb happens to be poised in unstable equi- librium on the edge of a tray or table, the developing tension may occasionally cause it to spring off as rigor supervenes. The author (BK) has seen athetoid writhing of the foot of a corpse, which lasted for 40 minutes, more than an hour after death.
There seems to be no doubt that some shortening does occur, but the noticeable effects are slight because both flexor and extensor muscle groups oppose each other across most limb joints. Bate-Smith and Bendall (1949) decided that shortening only occurred when there had been marked depletion of glycogen by activity before death, but Forster (1964) was of the opinion that, when a muscle was under some tension, it did shorten. His experiments showed that when the muscle was unloaded there was no change in length when rigor set in. Forster further showed that a high environ- mental temperature and poisons that increase muscle tone, such as parathion, lead to more shortening during rigor.
When fully established, rigor is ‘broken’ by forcible move- ments of the limbs or neck, then it will not return, a phe- nomenon utilized daily by mortuary staff and undertakers when preparing a body for a coffin. If rigor is still develop- ing, it will continue in the new posture of the limbs after they have been stretched. ‘Breaking’ fully established rigor is an accurate description, as the rigid, inelastic fibres are physically ruptured – sometimes tearing the muscle insertions from the bone. Rarely, rigor can assist in showing that a body has been moved between death and discovery. If an arm or leg is found projecting into free space without support, in a posture that obviously could not have been maintained dur- ing primary post-mortem flaccidity, then it must have been rolled over or otherwise moved. In these cases, a simple restorative movement (after the scene has been fully exam- ined) can usually indicate the original attitude quite simply.
Conversely, it can never be assumed that the posture of rigor in which a body is found was that which obtained at the time of death, as any amount of movement during the period of primary flaccidity will not be mirrored in the sub- sequent rigor.
Cadaveric spasm
This topic has received a disproportionate amount of notice in textbooks compared with its practical import- ance. No doubt this is because of its curiosity value rather than its usefulness. Cadaveric spasm is a rare form of virtu- ally instantaneous rigor that develops at the time of death with no period of post-mortem flaccidity.
Krompecher (1994), a major authority on rigor mortis, is extremely sceptical about the existence of true cadaveric
Rigor mortis
spasm, but many forensic pathologists claim to have seen such a phenomenon far too soon after death for it to be normal rigor mortis. The authors retain a healthy scepticism about the controversy, believing that most cases are misre- ported because of errors or uncertainties about the true time of death, so that early normal rigor could have supervened.
However, one or two cases within BK’s experience seem to be genuine enough to be remarkably early for true rigor.
It seems confined to those deaths that occur in the midst of intense physical and/or emotional activity, though how the latter can lead to instant post-mortem rigor is quite inex- plicable. It presumably must be initiated by motor nerve action, but for some reason there is a failure of the normal relaxation. The phenomenon usually affects only one group of muscles, such as the flexors of one arm, rather than the whole body.
It was shown in the earlier section on the biochemistry of rigor that marked depletion of glycogen stores in the muscle by violent exertion immediately before death can hasten the onset of muscular rigidity. Most cases of cadaveric spasm occur in similar circumstances and it was said to be particu- larly common on the battlefield amongst soldiers slain in combat. In the civilian sphere it is most often seen in per- sons who fall into water or drop some distance down a pre- cipitous slope such as a cliff. They may clutch at some nearby object, such as grass or shrubs, in an effort to break their fall and such material may be found held tightly in their fingers, even when the body is examined within a few minutes.
Another possibility, more common in detective fiction than in practice, is the gripping of a pistol with the finger still tightly flexed on the trigger, as evidence of true suicide rather than a ‘planted’ weapon in a homicide where an attempt has been made to simulate self-shooting. The chances of this actually being encountered by a pathologist are less than once in several professional lifetimes.
If found in the victim of drowning, or of a slide from a height, it has some value in confirming that the person was alive at the time of the fall, thus excluding the post-mortem disposal of an already dead body. Of course the body must be examined before ordinary rigor might be expected to have developed, or the presence of cadaveric spasm cannot then be assumed.
HEAT ANDCOLDSTIFFENING
At extremes of temperature the muscles may undergo a false rigor. In extreme cold, well below zero, once the intrinsic body heat is lost, the muscles may harden because the body fluids may freeze solid – as in the commercial or domestic preservation of meat in a freezing cabinet. The temperature has to be below –5°C for cold stiffening to occur and is usu- ally much lower. Part of the apparent stiffness is also due to solidification of the subcutaneous fat. When the body is warmed up, true rigor may supervene, though it may fail to appear as a result of intracellular damage caused by cell membranes being punctured by ice crystals.
Heat applied to the body also causes stiffness of the muscles, as the proteins of the tissues become denatured and coagulated as in cooking. The degree and depth of change depends on the intensity of the heat and the time for which it was applied. At autopsy the muscles may be shrivelled and desiccated, even carbonized on the surface. Beneath this there is a zone (which may be total) of brownish-pink
‘cooked meat’ and under that, if the process has not pene- trated, normal red muscle. Marked shortening occurs, caus- ing the well-known ‘pugilistic attitude’ of a burned body. This is because of the greater mass of flexor muscles com- pared with extensors, which forces the limbs into flexion and the spine into opisthotonus. These changes are purely post-mortem and are no indication of burning during life, as similar distortions occur during cremation.